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西田憲生

徳島大学

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2024年12月23日更新

職名: 准教授
電話: 研究者総覧に該当データはありませんでした。
電子メール: knishida@tokushima-u.ac.jp
学歴: ????/??: 京都府立医科大学医学科 ( - 2001. 3.)
2005/4: 徳島大学大学院医科学教育部プロテオミクス医科学専攻 ( - 2009. 3.)
学位: 博士(医学) (徳島大学)
職歴・経歴: 2011/10: 徳島大学助教, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/3: 徳島大学准教授, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/4: 徳島大学准教授, 大学院医歯薬学研究部

専門分野・研究分野: ライフサイエンス (Life sciences) [医療管理学、医療系社会学 (Healthcare management
medical sociology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
ライフサイエンス (Life sciences) [内科学一般 (Internal medicine - General)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
ライフサイエンス (Life sciences) [生理学 (Physiology)]

研究者総覧で最新データを確認する

2024年12月23日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [医療管理学、医療系社会学 (Healthcare management
medical sociology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
ライフサイエンス (Life sciences) [内科学一般 (Internal medicine - General)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
ライフサイエンス (Life sciences) [生理学 (Physiology)]
担当経験のある授業科目: CBT/OSCE (学部)
オリエンテーション(1年) (学部)
プレ配属演習 (学部)
医学概論 (共通教育)
医学研究実習(2年) (学部)
医学英語 (学部)
基礎医学 (学部)
基礎医学統合実習 (学部)
生理学 (学部)
生理学(Ⅰ・Ⅱ) (学部)
生理学Ⅰ・生理学Ⅰ実習 (学部)
臨床医学入門コース (学部)
臨床実習入門(講義) (学部)
指導経験: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年12月23日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [医療管理学、医療系社会学 (Healthcare management
medical sociology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
ライフサイエンス (Life sciences) [内科学一般 (Internal medicine - General)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
ライフサイエンス (Life sciences) [生理学 (Physiology)]

研究テーマ: 研究者総覧に該当データはありませんでした。

著書

西田憲生 :
ラクトバチルス・ガセリCP2305株の疲労軽減効果,
シーエムシー出版, 2020年4月. 西田憲生 :
腸内細菌叢を標的にした医薬品と保健機能食品の開発,
株式会社技術情報協会, 2018年9月.

論文

Kazuyoshi Noda, Yasushi Sato, Yasuyuki Okada, Kensei Nishida, Yutaka Kawano, Toshihito Tanahashi, Masahiro Bando, Koichi Okamoto, Masanori Takehara, Masahiro Sogabe, Hiroshi Miyamoto, Kei Daizumoto, Hiro-omi Kanayama and Tetsuji Takayama :
Exosomal miR-199a-3p Secreted From Cancer-Associated Adipocytes Promotes Pancreatic Cancer Progression.,
Cancer Medicine, Vol.13, No.20, e70265, 2024.

(要約): Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer. Recent studies indicated that cancer-associated adipocytes (CAAs) play crucial roles in tumor progression; however, the precise mechanism remains unknown. Here, we analyzed specific exosomal microRNAs (miRNA) signatures derived from pancreatic CAAs to investigate their role in cancer progression. CAAs were generated by co-culturing human adipocytes with human pancreatic cancer cells, and exosomes were isolated from the CAA-conditioned medium (CAA-CM). Small RNA-seq analysis was used to identify differentially expressed miRNAs in these exosomes. The effects of miRNAs on cell proliferation, migration/invasion, and drug sensitivity were examined. Luciferase reporter assays, real-time polymerase chain reaction, and western blotting were performed to investigate the molecular mechanisms of the miRNAs. The clinical relevance of the miRNAs was investigated using publicly available data and our cohort of patients with PDAC. miR-199a-3p expression was significantly increased in CAA-CM-derived exosomes. CAA-derived exosomes transferred miR-199a-3p to pancreatic cancer cells. Transfection with miR-199a-3p increased the proliferation, invasion, migration, and drug resistance of pancreatic cancer cells by downregulating SOCS7, increasing STAT3 phosphorylation, and upregulating SAA1 expression. High tissue miR-199a-3p expression is correlated with poor prognosis in patients with PDAC. Liquid biopsies revealed that exosomal miR-199a-3p could accurately differentiate patients with PDAC from healthy controls. Multivariate survival analysis indicated that miR-199a is an independent prognostic factor for PDAC. miR-199a-3p in CAA-derived exosomes contributes to the malignant transformation of pancreatic cancer via the SOCS7/STAT3/SAA1 pathway, suggesting its potential as a biomarker and therapeutic target for PDAC.
(キーワード): Humans / MicroRNAs / Exosomes / Pancreatic Neoplasms / Disease Progression / Cell Proliferation / Carcinoma, Pancreatic Ductal / Adipocytes / Cell Line, Tumor / Gene Expression Regulation, Neoplastic / Cell Movement / STAT3 Transcription Factor / Prognosis / Biomarkers, Tumor / Female / Male / Drug Resistance, Neoplasm
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cam4.70265
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39431622; ● Search Scopus @ Elsevier (PMID): 39431622; ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.70265

(DOI: 10.1002/cam4.70265, PubMed: 39431622) Noriaki Murayama, Koichi Okamoto, Tadahiko Nakagawa, Jinsei Miyoshi, Kensei Nishida, Tomoyuki Kawaguchi, kaizo kagemoto, Shinji Kitamura, Beibei Ma, Hiroshi Miyamoto, Naoki Muguruma, Mitsuyasu Yano, Koichi Tsuneyama, Takahiro Fujimori, Yasushi Sato and Tetsuji Takayama :
miR-144-3p/miR-451a promotes lymphovascular invasion through repression of PTEN/p19 in rectal neuroendocrine tumors.,
Journal of Gastroenterology and Hepatology, Vol.37, No.5, 919-927, 2022.

(要約): Although rectal neuroendocrine tumor (NET-G1) have potential metastatic capability, even among small tumors, no predictive biomarker for invasion and metastasis has been reported. We analyzed microRNA (miRNA) expression profiles in rectal NET-G1 tissues with and without lymphovascular invasion (LVI). Moreover, we then investigated their target genes to clarify the mechanism of invasion/metastasis in NET-G1. miRNA array analysis was performed using seven rectal NET-G1 tissues with LVI and seven without LVI. miRNA expression was confirmed by quantitative real-time PCR. A NET cell line H727 was transfected with miRNA mimic or target gene small interfering RNA, and migration and invasion assays were performed. The expression levels of miR-144-3p and miR-451a were significantly higher in NET-G1 with LVI versus without LVI, as determined by miRNA array analysis and RT-qPCR. A significant correlation was observed between miR-144-3p and miR-451a expression levels, strongly suggesting miR144/451 cluster overexpression in NET-G1 with LVI. Bioinformatic analysis of target genes revealed that miR-144-3p and miR-451a directly interact with PTEN and p19 mRNA, respectively. Immunohistochemistry revealed significantly lower expression of PTEN and p19 in NET-G1 tissues with LVI than in those without LVI. The miR-144-3p and miR-451a mimic significantly increased cell migration/invasion capability, respectively. Knockdown of PTEN and p19 induced significant augmentation of cell invasion and migration capability, respectively. Our data suggest that overexpression of miR-144/miR-451 cluster promotes LVI via repression of PTEN and p19 in rectal NET-G1 cells. miR-144/451 cluster may be a novel biomarker for predicting invasion/metastasis in rectal NET-G1.
(キーワード): Biomarkers / Cell Line, Tumor / Cell Movement / Cell Proliferation / Gene Expression Regulation, Neoplastic / Humans / MicroRNAs / Neuroendocrine Tumors / PTEN Phosphohydrolase / Rectal Neoplasms
(徳島大学機関リポジトリ): ● Metadata: 117699
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jgh.15833
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35332577; ● Search Scopus @ Elsevier (PMID): 35332577; ● Search Scopus @ Elsevier (DOI): 10.1111/jgh.15833

(徳島大学機関リポジトリ: 117699, DOI: 10.1111/jgh.15833, PubMed: 35332577) Akihiro Hirao, Yasushi Sato, Hironori Tanaka, Kensei Nishida, Tetsu Tomonari, Misato Hirata, Masahiro Bando, Yoshifumi Kida, Takahiro Tanaka, Tomoyuki Kawaguchi, Hironori Wada, Tatsuya Taniguchi, Koichi Okamoto, Hiroshi Miyamoto, Naoki Muguruma, Toshihito Tanahashi and Tetsuji Takayama :
MiR-125b-5p is Involved in Sorafenib Resistance through Ataxin-1-Mediated Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma.,
Cancers, Vol.13, No.19, 4917, 2021.

(要約): The mechanism of resistance to sorafenib in hepatocellular carcinoma (HCC) remains unclear. We analyzed miRNA expression profiles in sorafenib-resistant HCC cell lines (PLC/PRF5-R1/R2) and parental cell lines (PLC/PRF5) to identify the miRNAs responsible for resistance. Drug sensitivity, migration/invasion capabilities, and epithelial-mesenchymal transition (EMT) properties were analyzed by biochemical methods. The clinical relevance of the target genes to survival in HCC patients were assessed using a public database. Four miRNAs were significantly upregulated in PLC/PRF5-R1/-R2 compared with PLC/PRF5. Among them, miR-125b-5p mimic-transfected PLC/PRF5 cells (PLC/PRF5-miR125b) and showed a significantly higher IC50 for sorafenib compared with controls, while the other miRNA mimics did not. PLC/PRF5-miR125b showed lower E-cadherin and higher Snail and vimentin expression-findings similar to those for PLC/PRF5-R2-which suggests the induction of EMT in those cells. PLC/PRF5-miR125b exhibited significantly higher migration and invasion capabilities and induced sorafenib resistance in an in vivo mouse model. Bioinformatic analysis revealed ataxin-1 as a target gene of miR-125b-5p. PLC/PRF5 cells transfected with ataxin-1 siRNA showed a significantly higher IC50, higher migration/invasion capability, higher cancer stem cell population, and an EMT phenotype. Median overall survival in the low-ataxin-1 patient group was significantly shorter than in the high-ataxin-1 group. In conclusion, miR-125b-5p suppressed ataxin-1 and consequently induced Snail-mediated EMT and stemness, leading to a poor prognosis in HCC patients.
(徳島大学機関リポジトリ): ● Metadata: 116647
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers13194917
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34638401; ● Search Scopus @ Elsevier (PMID): 34638401; ● Search Scopus @ Elsevier (DOI): 10.3390/cancers13194917

(徳島大学機関リポジトリ: 116647, DOI: 10.3390/cancers13194917, PubMed: 34638401) Tatsuya Nishikawa, Yuki Kuwano, Mayu Nakata, Kazuhito Rokutan and Kensei Nishida :
Multiple G-quadruplexes in the LMNA promoter regulate LMNA variant 6 transcription and promote colon cancer cell growth.,
Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms, Vol.1864, No.10, 2021.

(要約): Lamin A/C proteins, major components of the nuclear lamina, are encoded by the LMNA gene. These proteins have multiple cellular functions, including DNA transcription and replication, chromatin organization, regulation of the cell cycle, and apoptosis. Mutations in LMNA are associated with a variety of diseases called laminopathies. LMNA has implications in cancer; however, its mechanisms of dysregulation in cancer cells are not yet fully understood. In this study, among the LMNA transcript variants, we focused on a transcriptional variant 6 (termed LMNA-V6), which contains unique 3 exons upstream of exon 1 of LMNA. The promoter region of LMNA-V6 formed multiple G-quadruplexes and increased its transcriptional activity. Moreover, LMNA-V6 negatively regulated other LMNA mRNA variants, lamin A and lamin C, via direct interaction with their promoter. Knockdown of LMNA-V6 decreased the proliferation of colon cancer cells, whereas overexpression of the unique 3 exons of LMNA-V6 increased cell growth. Furthermore, microarray gene expression profiling showed that alteration of LMNA-V6 levels influenced the expression of p53 in colon cancer cells. Taken together, the results suggest that LMNA-V6 may be a novel functional RNA whose expression is regulated through multiple G-quadruplexes in colon cancer cells.
(キーワード): Cell Line, Tumor / Cell Proliferation / Colonic Neoplasms / G-Quadruplexes / Gene Expression Regulation, Neoplastic / Humans / Lamin Type A / Promoter Regions, Genetic / RNA Isoforms / RNA Splicing / Transcription, Genetic
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbagrm.2021.194746
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34419630; ● Search Scopus @ Elsevier (PMID): 34419630; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbagrm.2021.194746

(DOI: 10.1016/j.bbagrm.2021.194746, PubMed: 34419630) Kensei Nishida, Daisuke Sawada, Toshiyuki Yasui, Yuki Kuwano and Kazuhito Rokutan :
Daily intake of Lactobacillus gasseri CP2305 ameliorates psychological premenstrual symptoms in young women: A randomized, double-blinded, placebo-controlled study,
Journal of Functional Foods, Vol.80, 104426, 2021.

(徳島大学機関リポジトリ): ● Metadata: 116456
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jff.2021.104426
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85102875111

(徳島大学機関リポジトリ: 116456, DOI: 10.1016/j.jff.2021.104426, Elsevier: Scopus) Kensei Nishida, Yuki Kuwano and Kazuhito Rokutan :
The MicroRNA-23b/27b/24 Cluster Facilitates Colon Cancer Cell Migration by Targeting FOXP2,
Cancers, Vol.12, No.1, 174, 2020.

(要約): Acquisition of cell migration capacity is an early and essential process in cancer development. The aim of this study was to identify microRNA gene expression networks that induced high migration capacity. Using colon cancer HCT116 cells subcloned by transwell-based migrated cell selection, microRNA array analysis was performed to examine the microRNA expression profile. Promoter activity and microRNA targets were assessed with luciferase reporters. Cell migration capacity was assessed by either the transwell or scratch assay. In isolated subpopulations with high migration capacity, the expression levels of the cluster increased in accordance with the increased expression of the short transcript, a host gene of the cluster. E2F1-binding sequences were involved in the basic transcription activity of the short expression, and E2F1-small-interfering (si)RNA treatment reduced the expression of both the and clusters. Overexpression experiments showed that and promoted cell migration, but the opposite effect was observed with . Forkhead box P2 (FOXP2) mRNA and protein levels were reduced by both/either and . Furthermore, FOXP2 siRNA treatment significantly promoted cell migration. Our findings demonstrated a novel role of the cluster in cell migration through targeting FOXP2, with potential implications for the development of microRNA-based therapy targeted at inhibiting cancer migration.
(徳島大学機関リポジトリ): ● Metadata: 114133
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cancers12010174
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31936744; ● Summary page in Scopus @ Elsevier: 2-s2.0-85078310271

(徳島大学機関リポジトリ: 114133, DOI: 10.3390/cancers12010174, PubMed: 31936744, Elsevier: Scopus) Kensei Nishida, Sawada Daisuke, Yuki Kuwano, Hiroki Tanaka and Kazuhito Rokutan :
Health Benefits of Lactobacillus gasseri CP2305 Tablets in Young Adults Exposed to Chronic Stress: A Randomized, Double-Blind, Placebo-Controlled Study,
Nutrients, Vol.11, No.8, 1859, 2019.

(要約): Short-term administration of CP2305 improves stress-associated symptoms and clinical symptoms in healthy young adults and in patients with irritable bowel syndrome, respectively. We evaluated the efficacy and health benefits of the long-term use of a tablet containing heat-inactivated, washed CP2305 (CP2305) in healthy young adults. Sixty Japanese medical students (41 men and 19 women) preparing for the national examination for medical practitioners ingested CP2305-containing or placebo tablets once daily for 24 weeks. Intake of the CP2305 tablet significantly reduced anxiety and sleep disturbance relative to placebo, as quantitated by the Spielberger State-Trait Anxiety Inventory and the Pittsburgh Sleep Quality Index. Single-channel sleep electroencephalograms show that CP2305 significantly shortened sleep latency and wake time after sleep onset and increased the delta power ratio in the first sleep cycle. CP2305 also significantly lowered salivary chromogranin A levels compared with placebo. Furthermore, 16S rRNA gene sequencing of participant feces demonstrated that CP2305 administration attenuated the stress-induced decline of spp. and the stress-induced elevation of spp. We conclude that the long-term use of CP2305-containing tablets may improve the mental state, sleep quality, and gut microbiota of healthy adults under stressful conditions.
(徳島大学機関リポジトリ): ● Metadata: 115658
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/nu11081859
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31405122; ● Search Scopus @ Elsevier (PMID): 31405122; ● Search Scopus @ Elsevier (DOI): 10.3390/nu11081859

(徳島大学機関リポジトリ: 115658, DOI: 10.3390/nu11081859, PubMed: 31405122) Tatsuya Nishikawa, Yuki Kuwano, Yumiko Takahara, Kensei Nishida and Kazuhito Rokutan :
HnRNPA1 interacts with G-quadruplex in the TRA2B promoter and stimulates its transcription in human colon cancer cells.,
Scientific Reports, Vol.9, No.1, 2019.

(要約): The human TRA2B gene consists of 10 exons and 9 introns and produces 5 splice isoforms (TRA2β1 to TRA2β5). TRA2B exon 2 encodes multiple premature termination codons. TRA2β1 lacks exon 2 and is translated into a functional transformer 2β (Tra2β) protein, whereas TRA2β4 contains 10 exons and works as a functional RNA. Overexpressed Tra2β and ectopic expression of TRA2β4 may be oncogenic. We found that heterogeneous nuclear ribonucleoprotein (hnRNP)A1 and hnRNPU interacted with TRA2β4 exon 2. Minigene assays revealed that hnRNPA1 facilitated inclusion of exon 2, whereas hnRNPU promoted its skipping. However, knockdown of hnRNPA1 or hnRNPU reduced both TRA2β1 and TRA2β4 levels, and overexpression of these hnRNPs increased levels of both isoforms, suggesting that hnRNPA1 and hnRNPU mainly regulate the transcription of TRA2B. In fact, hnRNPA1 and hnRNPU positively regulated the promoter activity of TRA2B. Circular dichroism analyses, electrophoretic mobility shift assays and chromatin immunoprecipitation assays demonstrated the presence of G-quadruplex (G4) formation in the promoter of TRA2B. Formation of G4 suppressed TRA2B transcription, whereas hnRNPA1, but not hnRNPU, interacted with the G4 to facilitate transcription. Our results suggest that hnRNPA1 may modulate TRA2B transcription through its regulation of G4 formation in its promoter in colon cancer cells.
(徳島大学機関リポジトリ): ● Metadata: 113781
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-019-46659-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31311954; ● Search Scopus @ Elsevier (PMID): 31311954; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-46659-x

(徳島大学機関リポジトリ: 113781, DOI: 10.1038/s41598-019-46659-x, PubMed: 31311954) Saki Saijo, Yuki Kuwano, Shoichiro Tange, Kazuhito Rokutan and Kensei Nishida :
A novel long non-coding RNA from the HOXA6-HOXA5 locus facilitates colon cancer cell growth.,
BMC Cancer, Vol.19, No.1, 2019.

(要約): Our results suggested that HOXA5 short RNA, a novel lncRNA, may play a crucial role in colon tumor growth through activation of EGF signaling.
(徳島大学機関リポジトリ): ● Metadata: 113406
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s12885-019-5715-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31159758; ● Search Scopus @ Elsevier (PMID): 31159758; ● Search Scopus @ Elsevier (DOI): 10.1186/s12885-019-5715-0

(徳島大学機関リポジトリ: 113406, DOI: 10.1186/s12885-019-5715-0, PubMed: 31159758) Daisuke Sawada, Yuki Kuwano, Hiroki Tanaka, Susumu Hara, Yoshihide Uchiyama, Tomonori Sugawara, Shigeru Fujiwara, Kazuhito Rokutan and Kensei Nishida :
Daily intake of Lactobacillus gasseri CP2305 relieves fatigue and stress-related symptoms in male university Ekiden runners: A double-blind, randomized, and placebo-controlled clinical trial,
Journal of Functional Foods, Vol.57, 465-476, 2019.

(徳島大学機関リポジトリ): ● Metadata: 115514
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jff.2019.04.022
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85064575794

(徳島大学機関リポジトリ: 115514, DOI: 10.1016/j.jff.2019.04.022, Elsevier: Scopus) Hiroki Tanaka, Yuki Kuwano, Tatsuya Nishikawa, Kazuhito Rokutan and Kensei Nishida :
promoter methylation accelerates colon cancer cell migration.,
Oncotarget, Vol.9, No.95, 36750-36769, 2018.

(要約): Diversification of transcriptomic and epigenomic states may occur during the expansion of colorectal cancers. Certain cancer cells lose their epithelial characters and gain mesenchymal properties, known as epithelial-mesenchymal transition (EMT), and they aggressively migrate into the non-tumorigenic extracellular matrix. In this study, we isolated a subpopulation with accelerated baseline motility (MG cells) and an immotile one (non-MG cells) from a colon cancer cell line (HCT116). Gene expression signatures of the MG cells indicated that this subpopulation was likely an EMT hybrid. The MG cells substantially lost their migratory properties after treatment with a methyltransferase inhibitor, 5-azacytidine, suggesting a role of DNA methylation in this process. Global transcriptome assays of both types of cells with or without 5-azacytidine treatment identified 640 genes, whose expression might be methylation-dependently down-regulated in the MG cells. Global methylation analysis revealed that 35 out of the 640 genes were hyper-methylated in the MG cells. Among them, we focused on the anti-oncogene ZNF350, which encodes a zinc-finger and BRCA1-interacting protein. Notably, ZNF350 knockdown accelerated migration of the non-MG cells, while overexpression of ZNF350 in the MG cells significantly impaired their migration. Finally, pyrosequence analysis together with dual luciferase assays of serially truncated fragments of the ZNF350 promoter (-268 to +49 bp) indicated that three hyper-methylated sites were possibly responsible for the basal promoter activity of ZNF350. Taken together, our results suggest that hyper-methylation of the ZNF350 proximal promoter may be one of the crucial determinants for acquiring increased migratory capabilities in colon cancer cells.
(徳島大学機関リポジトリ): ● Metadata: 113284
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.26353
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30613364; ● Summary page in Scopus @ Elsevier: 2-s2.0-85058059713

(徳島大学機関リポジトリ: 113284, DOI: 10.18632/oncotarget.26353, PubMed: 30613364, Elsevier: Scopus) Satake Yuzuru, Yuki Kuwano, Tatsuya Nishikawa, Fujita Kinuyo, Saijo Saki, Miki Itai, Tanaka Hiroki, Kensei Nishida and Kazuhito Rokutan :
Nucleolin facilitates nuclear retention of an ultraconserved region containing TRA24 and accelerates colon cancer cell growth.,
Oncotarget, Vol.9, No.42, 26817-26833, 2018.

(要約): Transcribed-ultraconserved regions (T-UCRs), which contain conserved sequences with 100% identity across human, rat and mouse species, are a novel category of functional RNAs. The human gene () encodes a UCR that spans exon 2 (276 bp) and its neighboring introns. Among five spliced RNA variants () transcribed from the gene, only contains the conserved exon 2. is overexpressed in colon cancer cells and accelerates cell growth by blocking the transcription of . However, the mechanisms underlying the overexpression of in colon cancer cells are unknown. Using biotinylated RNA pull-down assays followed by liquid chromatography-mass spectrometric analysis, we identified nucleolin as a -binding protein. Knockdown of nucleolin reduced the nuclear retention of and accelerated its degradation in the cytoplasm, whereas nucleolin overexpression increased levels and its mitogenic activity. Nucleolin directly bound to exon 2 via the glycine/arginine-rich (GAR) domain. Overexpression of GAR-deficient nucleolin failed to increase expression and growth of colon cancer cells. RNA fluorescence hybridization showed that co-localized with nucleolin in nuclei but not with the mutant lacking GAR. Our results suggest that specific interactions between nucleolin and UCR-containing may be associated with abnormal growth of colon cancer cells.
(徳島大学機関リポジトリ): ● Metadata: 112030
(出版サイトへのリンク): ● Publication site (DOI): 10.18632/oncotarget.25510
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29928487; ● Summary page in Scopus @ Elsevier: 2-s2.0-85047884974

(徳島大学機関リポジトリ: 112030, DOI: 10.18632/oncotarget.25510, PubMed: 29928487, Elsevier: Scopus) Miki Itai, Yuki Kuwano, Tatsuya Nishikawa, Kazuhito Rokutan and Kensei Nishida :
Geranylgeranylacetone prevents stress-induced decline of leptin secretion in mice.,
The Journal of Medical Investigation : JMI, Vol.65, No.1.2, 103-109, 2018.

(要約): Geranylgeranylacetone (GGA) is a chaperon inducer that protects various types of cell and tissue against stress. We examined whether GGA modulated energy intake and expenditure under stressful conditions. After mice were untreated or treated orally with GGA (0.16 g per kg body weight per day) for 10 days, they were subjected to 2-h restraint stress once or once a day for 5 consecutive days. GGA administration did not affect corticosterone response to the stress. Restraint stress rapidly decreased plasma leptin levels in control mice. GGA significantly increased circulating leptin levels without changing food intake and prevented the stress-induced decline of circulating leptin. However GGA-treated mice significantly reduced food intake during the repeated stress, compared with control mice. GGA prevented the stress-induced decline of leptin mRNA and its protein levels in epidydimal adipose tissues. We also found that GGA decreased ghrelin mRNA expression in gastric mucosa before the stress, whereas GGA-treated mice recovered the ghrelin mRNA expression to the baseline level after the repeated stress. Leptin and ghrelin are now recognized as regulators of anxiety and depressive mood. Our results suggest that GGA may regulate food intake and relief stress-induced mood disturbance through regulating leptin and ghrelin secretions. J. Med. Invest. 65:103-109, February, 2018.
(徳島大学機関リポジトリ): ● Metadata: 111438
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.65.103
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593178; ● Search Scopus @ Elsevier (PMID): 29593178; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.103

(徳島大学機関リポジトリ: 111438, DOI: 10.2152/jmi.65.103, PubMed: 29593178) Kensei Nishida, Sawada Daisuke, Tomoko Kawai, Yuki Kuwano, Fujiwara Shigeru and Kazuhito Rokutan :
Para-psychobiotic Lactobacillus gasseri CP2305 ameliorates stress-related symptoms and sleep quality.,
Journal of Applied Microbiology, Vol.123, No.6, 1561-1570, 2017.

(要約): Healthy students (21 males and 11 females) took paraprobiotic CP2305 daily for 5 weeks during a cadaver dissection course. The General Health Questionnaire and the Pittsburgh Sleep Quality Index were employed to assess stress-related somatic symptoms and sleep quality respectively. The aggravation of stress-associated somatic symptoms was observed in female students (P = 0·029). Sleep quality was improved in the paraprobiotic CP2305 group (P = 0·038), particularly in men (P = 0·004). Among men, paraprobiotic CP2305 shortened sleep latency (P = 0·035) and increased sleep duration (P = 0·048). Diarrhoea-like symptoms were also effectively controlled with CP2305 (P = 0·005) in men. Thus, we observed sex-related differences in the effects of paraprobiotic CP2305. In addition, CP2305 affected the growth of faecal Bacteroides vulgatus and Dorea longicatena, which are involved in intestinal inflammation.
(キーワード): Adult / Feces / Female / Humans / Lactobacillus gasseri / Male / Probiotics / Sex Factors / Sleep / Stress, Psychological / Students, Medical
(徳島大学機関リポジトリ): ● Metadata: 112974
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jam.13594
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28948675; ● Search Scopus @ Elsevier (PMID): 28948675; ● Search Scopus @ Elsevier (DOI): 10.1111/jam.13594

(徳島大学機関リポジトリ: 112974, DOI: 10.1111/jam.13594, PubMed: 28948675) Kensei Nishida, Daisuke Sawada, Yuki Kuwano, Hiroki Tanaka, Tomonori Sugawara, Yumeko Aoki, Shigeru Fujiwara and Kazuhito Rokutan :
Daily administration of paraprobiotic Lactobacillus gasseri CP2305 ameliorates chronic stress-associated symptoms in Japanese medical students.,
Journal of Functional Foods, Vol.36, 112-121, 2017.

(徳島大学機関リポジトリ): ● Metadata: 113030
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jff.2017.06.031
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85021772250

(徳島大学機関リポジトリ: 113030, DOI: 10.1016/j.jff.2017.06.031, Elsevier: Scopus) Shizue Masuki, Kensei Nishida, Shigenari Hashimoto, Mayuko Morikawa, Satoshi Takasugi, Masashi Nagata, Shun'ichiro Taniguchi, Kazuhito Rokutan and Hiroshi Nose :
Effects of milk product intake on thigh muscle strength and NFKB gene methylation during home-based interval walking training in older women: A randomized, controlled pilot study.,
PLoS ONE, Vol.12, No.5, e0176757, 2017.

(要約): Muscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women. Subjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week. After IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group. HD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women. UMIN-CTR No. UMIN000024544 and No. UMIN000024912.
(キーワード): Age Factors / Aged / Animals / Blood Cells / CpG Islands / DNA Methylation / Dairy Products / Exercise / Female / Gene Expression Profiling / Genome-Wide Association Study / Humans / Middle Aged / Milk / Muscle Strength / NF-kappa B / Patient Compliance / Physical Fitness / Pilot Projects / Promoter Regions, Genetic / Signal Transduction / Thigh / Time Factors / Walking
(徳島大学機関リポジトリ): ● Metadata: 112337
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0176757
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28520754; ● Search Scopus @ Elsevier (PMID): 28520754; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0176757

(徳島大学機関リポジトリ: 112337, DOI: 10.1371/journal.pone.0176757, PubMed: 28520754) Mai Takada, Kensei Nishida, Y. Gondo, H. Kikuchi-Hayakawa, H. Ishikawa, K. Suda, M. Kawai, R. Hoshi, Yuki Kuwano, K. Miyazaki and Kazuhito Rokutan :
Beneficial effects of Lactobacillus casei strain Shirota on academic stress-induced sleep disturbance in healthy adults: a double-blind, randomised, placebo-controlled trial.,
Beneficial Microbes, Vol.8, No.2, 153-162, 2017.

(要約): The present study examined whether Lactobacillus casei strain Shirota (LcS) improves sleep quality under psychological stress. A double-blind, placebo-controlled trial was conducted in healthy 4(th) year medical students exposed to academic examination stress. The trial was repeated over two consecutive years in different groups of students, and the data were pooled. For 8 weeks prior to and 3 weeks after a national standardised examination, a total of 48 and 46 subjects received a daily dose of 100 ml of LcS-fermented milk or non-fermented placebo milk, respectively. Study measures included subjective anxiety, overnight single-channel electroencephalography (EEG) recordings, and the Oguri-Shirakawa-Azumi (OSA) sleep inventory scores of subjective sleep quality. Total OSA scores were significantly lower than baseline on the day before the exam and recovered after the exam, indicating a stress-induced decline in sleep quality. There was a significant positive effect of LcS treatment on OSA factors for sleepiness on rising and sleep length. Sleep latency measured by EEG lengthened as the exam approached in the placebo group but was significantly suppressed in the LcS group. The percentage of stage 3 non-REM (N3) sleep decreased in the placebo group as the exam approached, whereas it was maintained in the LcS group throughout the trial. Delta power during the first sleep cycle, measured as an index of sleep intensity, increased as the exam approached in the LcS group and was significantly higher than in the placebo group. These findings suggest that daily consumption of LcS may help to maintain sleep quality during a period of increasing stress. The observed retention of N3 sleep and increased delta power in the LcS group may have contributed to higher perceived sleep satisfaction.
(出版サイトへのリンク): ● Publication site (DOI): 10.3920/BM2016.0150
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28443383; ● Search Scopus @ Elsevier (PMID): 28443383; ● Search Scopus @ Elsevier (DOI): 10.3920/BM2016.0150

(DOI: 10.3920/BM2016.0150, PubMed: 28443383) Daisuke Sawada, Tomoko Kawai, Kensei Nishida, Yuki Kuwano, Shigeru Fujiwara and Kazuhito Rokutan :
Daily intake of Lactobacillus gasseri CP2305 improves mental, physical, and sleep quality among Japanese medical students enrolled in a cadaver dissection course.,
Journal of Functional Foods, Vol.31, 188-197, 2017.

(徳島大学機関リポジトリ): ● Metadata: 113029
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jff.2017.01.042
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85011876409

(徳島大学機関リポジトリ: 113029, DOI: 10.1016/j.jff.2017.01.042, Elsevier: Scopus) Tomoko Kawai, Yuki Kuwano, Kiyoshi Masuda, Kinuyo Fujita, Hiroki Tanaka, Tatsuya Nishikawa, Kazuhito Rokutan and Kensei Nishida :
Adverse parenting is associated with blunted salivary cortisol awakening response and altered expression of glucocorticoid receptor and 2-adrenergic receptor mRNAs in leukocytes in Japanese medical students.,
Stress, Vol.20, No.2, 159-166, 2017.

(要約): Adverse parenting is associated with an increased risk for the development of mood and behavioral disorders. In this study, we assessed the perceived parental bonding of 232 medical students using the parental bonding instrument (PBI) and extracted 22 students who reported their parents' rearing attitudes as affectionless control (LOW; low care, high overprotection). Using the 28-item general health questionnaire, the Zung self-rating depression scale (Zung-SDS), the hospital anxiety and depression scale (HADS), and the Spielberger state-trait-anxiety-inventory (STAI), physical and mental state of the LOW students were compared with those of 30 students who reported their parental bonding as optimal (OPT; high care and low overprotection). These questionnaire measurements demonstrated significantly higher anxiety and depressive mood in the LOW students versus the OPT students. Compared with the OPT students, the LOW students also exhibited a significantly reduced salivary cortisol awakening response (CAR) without changes across the rest of the diurnal salivary cortisol profile. Among glucocorticoid-related genes examined (GR, ADRB2, IκBα, IL10, IL1R2, IL1RN, MR, MC2R, TGFB1, TGFB2 and FASLG), real-time reverse transcription-PCR showed that the LOW students significantly increased expression of a dominant negative glucocorticoid receptor β (GRβ) mRNA and decreased β2-adrenergic receptor (ADRB2) mRNA levels in circulating leukocytes. These results suggest that negative perception of parents' child-rearing attitudes may be associated with anxiety and depressive mood and altered glucocorticoid signaling even in healthy young adults.
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/10253890.2017.1297415
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28285561; ● Search Scopus @ Elsevier (PMID): 28285561; ● Search Scopus @ Elsevier (DOI): 10.1080/10253890.2017.1297415

(DOI: 10.1080/10253890.2017.1297415, PubMed: 28285561) Yasuteru Fujino, Shunsaku Takeishi, Kensei Nishida, Koichi Okamoto, Naoki Muguruma, Tetsuo Kimura, Shinji Kitamura, Hiroshi Miyamoto, Akiko Fujimoto, Jun Higashijima, Mitsuo Shimada, Kazuhito Rokutan and Tetsuji Takayama :
Downregulation of miR-100/miR-125b is associated with lymph node metastasis in early colorectal cancer with submucosal invasion.,
Cancer Science, Vol.108, No.3, 390-397, 2017.

(要約): A majority of early colorectal cancers (CRCs) with submucosal invasion undergo surgical operation, despite a very low incidence of lymph node metastasis. Our study aimed to identify microRNAs (miRNAs) specifically responsible for lymph node metastasis in submucosal CRCs. MicroRNA microarray analysis revealed that miR-100 and miR-125b expression levels were significantly lower in CRC tissues with lymph node metastases than in those without metastases. These results were validated by quantitative real-time PCR in a larger set of clinical samples. The transfection of a miR-100 or miR-125b inhibitor into colon cancer HCT116 cells significantly increased cell invasion, migration, and MMP activity. Conversely, overexpression of miR-100 or miR-125b mimics significantly attenuated all these activities but did not affect cell growth. To identify target mRNAs, we undertook a gene expression array analysis of miR-100-silenced HCT116 cells as well as negative control cells. The Ingenuity Pathway Analysis, TargetScan software analyses, and subsequent verification of mRNA expression by real-time PCR identified mammalian target of rapamycin (mTOR) and insulin-like growth factor 1 receptor (IGF1R) as direct, and Fas and X-linked inhibitor-of-apoptosis protein (XIAP) as indirect candidate targets for miR-100 involved in lymph node metastasis. Knockdown of each gene by siRNA significantly reduced the invasiveness of HCT116 cells. These data clearly show that downregulation of miR-100 and miR-125b is closely associated with lymph node metastasis in submucosal CRC through enhancement of invasion, motility, and MMP activity. In particular, miR-100 may promote metastasis by upregulating mTOR, IGF1R, Fas, and XIAP as targets. Thus, miR-100 and miR-125b may be novel biomarkers for lymph node metastasis of early CRCs with submucosal invasion.
(キーワード): Antigens, CD95 / Cell Line, Tumor / Cell Movement / Cell Proliferation / Colorectal Neoplasms / HCT116 Cells / HT29 Cells / Humans / Lymphatic Metastasis / Matrix Metalloproteinases / MicroRNAs / RNA Interference / RNA, Small Interfering / Receptors, Somatomedin / TOR Serine-Threonine Kinases / X-Linked Inhibitor of Apoptosis Protein
(徳島大学機関リポジトリ): ● Metadata: 112375
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cas.13152
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28032929; ● Search Scopus @ Elsevier (PMID): 28032929; ● Search Scopus @ Elsevier (DOI): 10.1111/cas.13152

(徳島大学機関リポジトリ: 112375, DOI: 10.1111/cas.13152, PubMed: 28032929) K. Nobutani, Daisuke Sawada, Shiferu Fujiwara, Yuki Kuwano, Kensei Nishida, J. Nakayama, H. Kutsumi, T. Azuma and Kazuhito Rokutan :
The effects of administration of the Lactobacillus gasseri strain CP2305 on quality of life, clinical symptoms and changes in gene expression in patients with irritable bowel syndrome.,
Journal of Applied Microbiology, Vol.122, No.1, 212-224, 2017.

(要約): To clarify the effects of Lactobacillus gasseri CP2305 (CP2305) on quality of life and clinical symptoms and its functional mechanisms in patients with irritable bowel syndrome (IBS). After the patients were administered CP2305 daily for 4 weeks, the IBS-severity index score was significantly improved compared with that of the placebo group, and this improvement was accompanied by a reduction in health-related worry and changes in intestinal microbiota. The gene expression profiling of the peripheral blood leucocytes showed that CP2305 treatment significantly up-regulated genes related to eukaryotic initiation factor 2 (EIF2) signalling. Eighty-two genes were down-regulated in IBS patients compared with healthy controls. The expression of 23 of these genes exhibited a CP2305-dependent increase associated with an improvement in IBS severity. The majority of the restored genes were related to EIF2 signalling. CP2305 administration is a potential candidate therapeutic option for patients with IBS. Although probiotics have been proposed to benefit IBS patients, objective clinical evidence and elucidation of the functional mechanism remain insufficient. Our study demonstrated that CP2305 administration beneficially influences IBS patients in both subjective and objective evaluations, and gene expression profiling provided insights into the functional mechanism.
(キーワード): Adult / Female / Humans / Irritable Bowel Syndrome / Lactobacillus gasseri / Male / Middle Aged / Probiotics / Quality of Life / Treatment Outcome
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jam.13329
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27761980; ● Search Scopus @ Elsevier (PMID): 27761980; ● Search Scopus @ Elsevier (DOI): 10.1111/jam.13329

(DOI: 10.1111/jam.13329, PubMed: 27761980) Kinuyo Fujita, Yuki Kuwano, Saki Saijo, Tatsuya Nishikawa, Kensei Nishida and Kazuhito Rokutan :
Negative perception of socioeconomic status with depressive mood down-regulates expression of PPBP and SLC1A7 genes in peripheral blood leukocytes.,
Cogent Psychology, Vol.4, No.1, 1338825, 2017.

(徳島大学機関リポジトリ): ● Metadata: 111435
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/23311908.2017.1338825
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1080/23311908.2017.1338825

(徳島大学機関リポジトリ: 111435, DOI: 10.1080/23311908.2017.1338825) Yuki Kuwano, Kensei Nishida, Yoko Akaike, Ken Kurokawa, Tatsuya Nishikawa, Kiyoshi Masuda and Kazuhito Rokutan :
Homeodomain-Interacting Protein Kinase-2: A Critical Regulator of the DNA Damage Response and the Epigenome.,
International Journal of Molecular Sciences, Vol.17, No.10, 2016.

(要約): Homeodomain-interacting protein kinase 2 (HIPK2) is a serine/threonine kinase that phosphorylates and activates the apoptotic program through interaction with diverse downstream targets including tumor suppressor p53. HIPK2 is activated by genotoxic stimuli and modulates cell fate following DNA damage. The DNA damage response (DDR) is triggered by DNA lesions or chromatin alterations. The DDR regulates DNA repair, cell cycle checkpoint activation, and apoptosis to restore genome integrity and cellular homeostasis. Maintenance of the DDR is essential to prevent development of diseases caused by genomic instability, including cancer, defects of development, and neurodegenerative disorders. Recent studies reveal a novel HIPK2-mediated pathway for DDR through interaction with chromatin remodeling factor homeodomain protein 1. In this review, we will highlight the molecular mechanisms of HIPK2 and show its functions as a crucial DDR regulator.
(徳島大学機関リポジトリ): ● Metadata: 112409
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/ijms17101638
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27689990; ● Summary page in Scopus @ Elsevier: 2-s2.0-84989282554

(徳島大学機関リポジトリ: 112409, DOI: 10.3390/ijms17101638, PubMed: 27689990, Elsevier: Scopus) Akito Kato-Kataoka, Kensei Nishida, Mai Takada, Mitsuhisa Kawai, Hiroko Kikuchi-Hayakawa, Kazunori Suda, Hiroshi Ishikawa, Yusuke Gondo, Kensuke Shimizu, Takahiro Matsuki, Akira Kushiro, Ryoutaro Hoshi, Osamu Watanabe, Tomoki Igarashi, Kouji Miyazaki, Yuki Kuwano and Kazuhito Rokutan :
Fermented Milk Containing Lactobacillus casei Strain Shirota Preserves the Diversity of the Gut Microbiota and Relieves Abdominal Dysfunction in Healthy Medical Students Exposed to Academic Stress.,
Applied and Environmental Microbiology, Vol.82, No.12, 3649-3658, 2016.

(要約): A novel clinical trial was conducted with healthy medical students under examination stress conditions. It was demonstrated that the daily consumption of lactic acid bacteria provided health benefits to prevent the onset of stress-associated abdominal symptoms and a good change of gut microbiota in healthy medical students.
(出版サイトへのリンク): ● Publication site (DOI): 10.1128/AEM.04134-15
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27208120; ● Search Scopus @ Elsevier (PMID): 27208120; ● Search Scopus @ Elsevier (DOI): 10.1128/AEM.04134-15

(DOI: 10.1128/AEM.04134-15, PubMed: 27208120) K Kajita, Yuki Kuwano, Y Satake, S Kano, K Kurokawa, Y Akaike, Kiyoshi Masuda, Kensei Nishida and Kazuhito Rokutan :
Ultraconserved region-containing Transformer 24 controls senescence of colon cancer cells.,
Oncogenesis, Vol.5, 2016.

(徳島大学機関リポジトリ): ● Metadata: 110161
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/oncsis.2016.18
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27043659; ● Search Scopus @ Elsevier (PMID): 27043659; ● Search Scopus @ Elsevier (DOI): 10.1038/oncsis.2016.18

(徳島大学機関リポジトリ: 110161, DOI: 10.1038/oncsis.2016.18, PubMed: 27043659) M Takada, Kensei Nishida, A Kataoka-Kato, Y Gondo, H Ishikawa, K Suda, M Kawai, R Hoshi, O Watanabe, T Igarashi, Yuki Kuwano, K Miyazaki and Kazuhito Rokutan :
Probiotic Lactobacillus casei strain Shirota relieves stress-associated symptoms by modulating the gut-brain interaction in human and animal models.,
Neurogastroenterology and Motility, 2016.

(出版サイトへのリンク): ● Publication site (DOI): 10.1111/nmo.12804
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26896291; ● Summary page in Scopus @ Elsevier: 2-s2.0-84977109319

(DOI: 10.1111/nmo.12804, PubMed: 26896291, Elsevier: Scopus) T. Kawamura, K. Uno, K. Tanaka, Y. Ueda, N. Sakiyama, Kensei Nishida, Kazuhito Rokutan and K. Yasuda :
Morphological Characteristics and Location of Missed, Advanced Colorectal Neoplasms after Colonoscopy.,
The Journal of Medical Investigation : JMI, Vol.63, No.3-4, 163-170, 2016.

(要約): This retrospective study aimed to clarify the clinical characteristics of advanced colorectal neoplasms after colonoscopy, likely to have been missed on the previous colonoscopy. We reviewed a total of 5,768 consecutive colonoscopies performed from April 2010 to September 2013 in 4,841 patients, and analyzed advanced colorectal neoplasms after colonoscopy, particularly focusing on their morphological characteristics and locations, as compared with primary lesions, defined as lesions detected in their first colonoscopy or in a subsequent colonoscopy >5 years after the previous one. Of the 5,768 examinations, 922 advanced neoplasms (including 217 cancers with ≥T2) were detected, and 167 lesions (18.1%) were diagnosed within 5 years after a previous colonoscopy (post-colonoscopy advanced neoplasms). The incidence of right-sided lesions in the post-colonoscopy advanced neoplasms (48.5%, 81/167) was significantly higher than in the primary lesions (34.0%, 257/755; p <0.001). We excluded 217 cancers with ≥T2 from the morphological analysis to characterize early-stage post-colonoscopy advanced neoplasms. The incidence of non-polypoid lesions in the post-colonoscopy advanced neoplasms (25.6%, 41/160) was significantly higher than that in the primary lesions (12.3%, 67/545; p <0.001). These findings suggest that extra attention should be paid to non-polypoid, right-sided advanced colorectal neoplasms during screening and surveillance colonoscopy. J. Med. Invest. 63: 163-170, August, 2016.
(キーワード): Aged / Aged, 80 and over / Colonoscopy / Colorectal Neoplasms / Female / Humans / Male / Middle Aged / Retrospective Studies
(徳島大学機関リポジトリ): ● Metadata: 111172
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.63.163
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27644552; ● Search Scopus @ Elsevier (PMID): 27644552; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.63.163

(徳島大学機関リポジトリ: 111172, DOI: 10.2152/jmi.63.163, PubMed: 27644552) Saki Saijo, Yuki Kuwano, Kiyoshi Masuda, Tatsuya Nishikawa, Kazuhito Rokutan and Kensei Nishida :
Serine/arginine-rich splicing factor 7 regulates p21-dependent growth arrest in colon cancer cells.,
The Journal of Medical Investigation : JMI, Vol.63, No.3-4, 219-226, 2016.

(要約): Serine/arginine-rich splicing factors (SRSFs) play wide-ranging roles in gene expression through post-transcriptional regulation as well as pre-mRNA splicing. SRSF7 was highly expressed in colon cancer tissues, and its knockdown inhibited cell growth in colon cancer cells (HCT116) in association with altered expression of 4,499 genes. The Ingenuity Pathway Analysis revealed that cell cycle-related canonical pathways were ranked as the highly enriched category in the affected genes. Western blotting confirmed that p21, a master regulator in cell cycle, was increased without any induction of p53 in SRSF7 knockdown cells. Furthermore, cyclin-dependent kinase 2 and retinoblastoma protein were remained in the hypophosphorylated state. In addition, the SRSF7 knockdown-induced cell growth inhibition was observed in p53-null HCT116 cells, suggesting that p53-independent pathways were involved in the SRSF7 knockdown-induced cell growth inhibition. The reduction of SRSF7 stabilized cyclin-dependent kinase inhibitor 1A (CDKN1A) mRNA without any activation of the CDKN1A promoter. Interestingly, SRSF7 knockdown also blocked p21 degradation. These results suggest that the reduction of SRSF7 post-transcriptionally regulates p21 induction at the multistep processes. Thus, the present findings disclose a novel, important role of SRSF7 in cell proliferation through regulating p21 levels. J. Med. Invest. 63: 219-226, August, 2016.
(キーワード): Cell Proliferation / Colonic Neoplasms / Cyclin-Dependent Kinase Inhibitor p21 / HCT116 Cells / Humans / RNA, Messenger / Serine-Arginine Splicing Factors / Tumor Suppressor Protein p53
(徳島大学機関リポジトリ): ● Metadata: 110162
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.63.219
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27644562; ● Search Scopus @ Elsevier (PMID): 27644562; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.63.219

(徳島大学機関リポジトリ: 110162, DOI: 10.2152/jmi.63.219, PubMed: 27644562) A Kato-Kataoka, Kensei Nishida, M Takada, K Suda, M Kawai, K Shimizu, A Kushiro, R Hoshi, O Watanabe, T Igarashi, K Miyazaki, Yuki Kuwano and Kazuhito Rokutan :
Fermented milk containing Lactobacillus casei strain Shirota prevents the onset of physical symptoms in medical students under academic examination stress.,
Beneficial Microbes, Vol.7, No.2, 153-156, 2016.

(要約): This pilot study investigated the effects of the probiotic Lactobacillus casei strain Shirota (LcS) on psychological, physiological, and physical stress responses in medical students undertaking an authorised nationwide examination for promotion. In a double-blind, placebo-controlled trial, 24 and 23 healthy medical students consumed a fermented milk containing LcS and a placebo milk, respectively, once a day for 8 weeks until the day before the examination. Psychophysical state, salivary cortisol, faecal serotonin, and plasma L-tryptophan were analysed on 5 different sampling days (8 weeks before, 2 weeks before, 1 day before, immediately after, and 2 weeks after the examination). Physical symptoms were also recorded in a diary by subjects during the intervention period for 8 weeks. In association with a significant elevation of anxiety at 1 day before the examination, salivary cortisol and plasma L-tryptophan levels were significantly increased in only the placebo group (P<0.05). Two weeks after the examination, the LcS group had significantly higher faecal serotonin levels (P<0.05) than the placebo group. Moreover, the rate of subjects experiencing common abdominal and cold symptoms and total number of days experiencing these physical symptoms per subject were significantly lower in the LcS group than in the placebo group during the pre-examination period at 5-6 weeks (each P<0.05) and 7-8 weeks (each P<0.01) during the intervention period. Our results suggest that the daily consumption of fermented milk containing LcS may exert beneficial effects preventing the onset of physical symptoms in healthy subjects exposed to stressful situations.
(出版サイトへのリンク): ● Publication site (DOI): 10.3920/BM2015.0100
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26689231; ● Search Scopus @ Elsevier (PMID): 26689231; ● Search Scopus @ Elsevier (DOI): 10.3920/BM2015.0100

(DOI: 10.3920/BM2015.0100, PubMed: 26689231) Yuki Kuwano, Kensei Nishida, Keisuke Kajita, Yuzuru Satake, Yoko Akaike, Kiyuyo Fujita, Shizuka Kano, Kiyoshi Masuda and Kazuhito Rokutan :
Transformer 2 and miR-204 regulate apoptosis through competitive binding to 3 UTR of BCL2 mRNA,
Cell Death and Differentiation, Vol.22, No.5, 815-825, 2015.

(要約): RNA-binding proteins and microRNAs are potent post-transcriptional regulators of gene expression. Human transformer 2β (Tra2β) is a serine/arginine-rich-like protein splicing factor and is now implicated to have wide-ranging roles in gene expression as an RNA-binding protein. RNA immunoprecipitation (RIP) with an anti-Tra2β antibody and microarray analysis identified a subset of Tra2β-associated mRNAs in HCT116 human colon cancer cells, many of which encoded cell death-related proteins including Bcl-2 (B-cell CLL/lymphoma 2). Tra2β knockdown in HCT116 cells decreased Bcl-2 expression and induced apoptosis. Tra2β knockdown accelerated the decay of BCL2α mRNA that encodes Bcl-2 and full-length 3' UTR, while it did not affect the stability of BCL2β mRNA having a short, alternatively spliced 3' UTR different from BCL2α 3' UTR. RIP assays with anti-Tra2β and anti-Argonaute 2 antibodies, respectively, showed that Tra2β bound to BCL2α 3' UTR, and that Tra2β knockdown facilitated association of miR-204 with BCL2α 3' UTR. The consensus sequence (GAA) for Tra2β-binding lies within the miR-204-binding site of BCL2 3' UTR. Mutation of the consensus sequence canceled the binding of Tra2β to BCL2 3' UTR without disrupting miR-204-binding to BCL2 3' UTR. Transfection of an anti-miR-204 or introduction of three-point mutations into the miR-204-binding site increased BCL2 mRNA and Bcl-2 protein levels. Inversely, transfection of precursor miR-204 reduced their levels. Experiments with Tra2β-silenced or overexpressed cells revealed that Tra2β antagonized the effects of miR-204 and upregulated Bcl-2 expression. Furthermore, TRA2β mRNA expression was significantly upregulated in 22 colon cancer tissues compared with paired normal tissues and positively correlated with BCL2 mRNA expression. Tra2β knockdown in human lung adenocarcinoma cells (A549) increased their sensitivity to anticancer drugs. Taken together, our findings suggest that Tra2β regulates apoptosis by modulating Bcl-2 expression through its competition with miR-204. This novel function may have a crucial role in tumor growth.
(キーワード): 3' Untranslated Regions / Alternative Splicing / Apoptosis / Colonic Neoplasms / HEK293 Cells / HeLa Cells / Humans / MicroRNAs / Nerve Tissue Proteins / Proto-Oncogene Proteins c-bcl-2 / RNA, Neoplasm / RNA-Binding Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/cdd.2014.176
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25342468; ● Summary page in Scopus @ Elsevier: 2-s2.0-84928340238

(DOI: 10.1038/cdd.2014.176, PubMed: 25342468, Elsevier: Scopus) Y Akaike, Yuki Kuwano, Kensei Nishida, K Kurokawa, K Kajita, S Kano, Kiyoshi Masuda and Kazuhito Rokutan :
Homeodomain-interacting protein kinase 2 regulates DNA damage response through interacting with heterochromatin protein 1.,
Oncogene, Vol.34, No.26, 3463-3473, 2014.

(要約): Homeodomain-interacting protein kinase 2 (HIPK2) is a potential tumor suppressor that has a crucial role in the DNA damage response (DDR) by regulating cell-cycle checkpoint activation and apoptosis. However, it is unclear whether HIPK2 exerts distinct roles in DNA damage repair. The aim of this study was to identify novel target molecule(s) of HIPK2, which mediates HIPK2-dependent DNA damage repair. HIPK2-knockdown human colon cancer cells (HCT116) or hipk1/hipk2 double-deficient mouse embryonic fibroblasts could not remove histone H2A.X phosphorylated at Ser139 (γH2A.X) after irradiation with a sublethal dose (10 J/m(2)) of ultraviolet (UV)-C, resulting in apoptosis. Knockdown of HIPK2 in p53-null HCT116 cells similarly promoted the UV-C-induced γH2A.X accumulation and apoptosis. Proteomic analysis of HIPK2-associated proteins using liquid chromatography-tandem mass spectrometry identified heterochromatin protein 1γ (HP1γ) as a novel target for HIPK2. Immunoprecipitation experiments with HCT116 cells expressing FLAG-tagged HIPK2 and one of the HA-tagged HP1 family members demonstrated that HIPK2 specifically associated with HP1γ, but not with HP1α or HP1β, through its chromo-shadow domain. Mutation of the HP1box motif (883-PTVSV-887) within HIPK2 abolished the association. HP1γ knockdown also enhanced accumulation of γH2A.X and apoptosis after sublethal UV-C irradiation. In vitro kinase assay demonstrated an HP1γ-phosphorylating activity of HIPK2. Sublethal UV-C irradiation phosphorylated HP1γ. This phosphorylation was absent in endogenous HIPK2-silenced cells with HIPK2 3'UTR siRNA. Overexpression of FLAG-HIPK2, but not the HP1box-mutated or kinase-dead HIPK2 mutant, in the HIPK2-silenced cells increased HP1γ binding to trimethylated (Lys9) histone H3 (H3K9me3), rescued the UV-C-induced phosphorylation of HP1γ, triggered release of HP1γ from histone H3K9me3 and suppressed γH2A.X accumulation. Our results suggest that HIPK2-dependent phosphorylation of HP1γ may participate in the regulation of dynamic interaction between HP1γ and histone H3K9me3 to promote DNA damage repair. This HIPK2/HP1γ pathway may uncover a new functional aspect of HIPK2 as a tumor suppressor.
(徳島大学機関リポジトリ): ● Metadata: 106072
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/onc.2014.278
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25151962; ● Summary page in Scopus @ Elsevier: 2-s2.0-84933053342

(徳島大学機関リポジトリ: 106072, DOI: 10.1038/onc.2014.278, PubMed: 25151962, Elsevier: Scopus) Yoko Akaike, Kiyoshi Masuda, Yuki Kuwano, Kensei Nishida, Keisuke Kajita, Ken Kurokawa, Yuzuru Satake, Katsutoshi Shoda, Issei Imoto and Kazuhito Rokutan :
HuR Regulates Alternative Splicing of the TRA2 Gene in Human Colon Cancer Cells under Oxidative Stress.,
Molecular and Cellular Biology, Vol.34, No.15, 2857-2873, 2014.

(要約): Hu antigen R (HuR) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs. The human TRA2 gene encodes splicing factor transformer 2 (Tra2) and generates 5 mRNA isoforms (TRA21 to -5) through alternative splicing. Exposure of HCT116 colon cancer cells to sodium arsenite stimulated checkpoint kinase 2 (Chk2)- and mitogen-activated protein kinase p38 (p38(MAPK))-mediated phosphorylation of HuR at positions S88 and T118. This induced an association between HuR and the 39-nucleotide (nt) proximal region of TRA2 exon 2, generating a TRA24 mRNA that includes exon 2, which has multiple premature stop codons. HuR knockdown or Chk2/p38(MAPK) double knockdown inhibited the arsenite-stimulated production of TRA24 and increased Tra2 protein, facilitating Tra2-dependent inclusion of exons in target pre-mRNAs. The effects of HuR knockdown or Chk2/p38(MAPK) double knockdown were also confirmed using a TRA2 minigene spanning exons 1 to 4, and the effects disappeared when the 39-nt region was deleted from the minigene. In endogenous HuR knockdown cells, the overexpression of a HuR mutant that could not be phosphorylated (with changes of serine to alanine at position 88 [S88A], S100A, and T118A) blocked the associated TRA24 interaction and TRA24 generation, while the overexpression of a phosphomimetic HuR (with mutations S88D, S100D, and T118D) restored the TRA24-related activities. Our findings revealed the potential role of nuclear HuR in the regulation of alternative splicing programs under oxidative stress.
(出版サイトへのリンク): ● Publication site (DOI): 10.1128/MCB.00333-14
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24865968; ● Summary page in Scopus @ Elsevier: 2-s2.0-84904288500

(DOI: 10.1128/MCB.00333-14, PubMed: 24865968, Elsevier: Scopus) Ken Kurokawa, Yoko Akaike, Kiyoshi Masuda, Yuki Kuwano, Kensei Nishida, Naoko Yamagishi, Keisuke Kajita, Toshihito Tanahashi and Kazuhito Rokutan :
Downregulation of serine/arginine-rich splicing factor 3 induces G1 cell cycle arrest and apoptosis in colon cancer cells,
Oncogene, Vol.33, No.11, 1407-1417, 2014.

(要約): Serine/arginine-rich splicing factor 3 (SRSF3) likely has wide-ranging roles in gene expression and facilitation of tumor cell growth. SRSF3 knockdown induced G1 arrest and apoptosis in colon cancer cells (HCT116) in association with altered expression of 833 genes. Pathway analysis revealed 'G1/S Checkpoint Regulation' as the most highly enriched category in the affected genes. SRSF3 knockdown did not induce p53 or stimulate phosphorylation of p53 or histone H2A.X in wild-type HCT116 cells. Furthermore, the knockdown induced G1 arrest in p53-null HCT116 cells, suggesting that p53-dependent DNA damage responses did not mediate the G1 arrest. Real-time reverse transcription-polymerase chain reaction and western blotting confirmed that SRSF3 knockdown reduced mRNA and protein levels of cyclins (D1, D3 and E1), E2F1 and E2F7. The decreased expression of cyclin D and E2F1 likely impaired the G1-to-S-phase progression. Consequently, retinoblastoma protein remained hypophosphorylated in SRSF3 knockdown cells. The knockdown also induced apoptosis in association with reduction of BCL2 protein levels. We also found that SRSF3 knockdown facilitated skipping of 81 5'-nucleotides (27 amino acids) from exon 8 of homeodomain-interacting protein kinase-2 (HIPK2) and produced a HIPK2 Δe8 isoform. Full-length HIPK2 (HIPK2 FL) is constantly degraded through association with an E3 ubiquitin ligase (Siah-1), whereas HIPK2 Δe8, lacking the 27 amino acids, lost Siah-1-binding ability and became resistant to proteasome digestion. Interestingly, selective knockdown of HIPK2 FL induced apoptosis in various colon cancer cells expressing wild-type or mutated p53. Thus, these findings disclose an important role of SRSF3 in the regulation of the G1-to-S-phase progression and alternative splicing of HIPK2 in tumor growth.
(キーワード): Alternative Splicing / Apoptosis / Colonic Neoplasms / Down-Regulation / G1 Phase / Humans / RNA-Binding Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/onc.2013.86
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23503458; ● Summary page in Scopus @ Elsevier: 2-s2.0-84896395111

(DOI: 10.1038/onc.2013.86, PubMed: 23503458, Elsevier: Scopus) Shizuka Kano, Kensei Nishida, Hiroyuki Kurebe, Chihiro Nishiyama, Kentaro Kita, Yoko Akaike, Keisuke Kajita, Ken Kurokawa, Kiyoshi Masuda, Yuki Kuwano, Toshihito Tanahashi and Kazuhito Rokutan :
Oxidative stress-inducible truncated serine/arginine-rich splicing factor 3 regulates interleukin-8 production in human colon cancer cells,
American Journal of Physiology, Cell Physiology, Vol.306, No.3, C250-C262, 2014.

(要約): Serine/arginine-rich splicing factor 3 (SRSF3) is a member of the SR protein family and plays wide-ranging roles in gene expression. The human SRSF3 gene generates two alternative splice transcripts, a major mRNA isoform (SRSF3-FL) encoding functional full-length protein and a premature termination codon (PTC)-containing isoform (SRSF3-PTC). The latter is degraded through nonsense-mediated mRNA decay (NMD). Treatment of a human colon cancer cell line (HCT116) with 100 μM sodium arsenite increased SRSF3-PTC mRNA levels without changing SRSF3-FL mRNA levels. A chemiluminescence-based NMD reporter assay system demonstrated that arsenite treatment inhibited NMD activity and increased SRSF3-PTC mRNA levels in the cytoplasm, facilitating translation of a truncated SRSF3 protein (SRSF3-TR) from SRSF3-PTC mRNA. SRSF3-TR lacked two-thirds of the Arg/Ser-rich (RS) domain whose phosphorylation state is known to be crucial for subcellular distribution. SRSF3-FL was localized in the nucleus, while overexpressed SRSF3-TR was diffusely distributed in the cytoplasm and the nucleus. A part of SRSF3-TR was also associated with stress granules in the cytoplasm. Interestingly, treatment of HCT116 cells with a small interference RNA specifically targeting SRSF3-PTC mRNA significantly attenuated arsenite-stimulated induction of c-JUN protein, its binding activity to the AP-1 binding site (-126 to 120 bp) in the interleukin (IL)-8 gene promoter, and AP-1 promoter activity, resulting in significant reduction of arsenite-stimulated IL-8 production. Our results suggest that SRSF3-TR may function as a positive regulator of oxidative stress-initiated inflammatory responses in colon cancer cells.
(キーワード): Alternative Splicing / Arsenites / Binding Sites / Cell Line, Tumor / Codon, Nonsense / Colonic Neoplasms / Gene Expression Regulation, Neoplastic / HCT116 Cells / Humans / Interleukin-8 / Nonsense Mediated mRNA Decay / Oxidative Stress / Promoter Regions, Genetic / Protein Binding / Protein Isoforms / Protein Structure, Tertiary / Proto-Oncogene Proteins c-jun / RNA Interference / RNA, Small Interfering / RNA-Binding Proteins / Sodium Compounds / Transcription Factor AP-1
(徳島大学機関リポジトリ): ● Metadata: 109685
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpcell.00091.2013
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24284797; ● Summary page in Scopus @ Elsevier: 2-s2.0-84893370362

(徳島大学機関リポジトリ: 109685, DOI: 10.1152/ajpcell.00091.2013, PubMed: 24284797, Elsevier: Scopus) Keisuke Kajita, Yuki Kuwano, Naruka Kitamura, Yuzuru Satake, Kensei Nishida, Ken Kurokawa, Yoko Akaike, Manami Honda, Kiyoshi Masuda and Kazuhito Rokutan :
Ets1 and heat shock factor 1 regulate transcription of the Transformer 2β gene in human colon cancer cells,
Journal of Gastroenterology, Vol.48, No.11, 1222-1233, 2013.

(要約): Transformer (Tra) 2β is a member of the serine/arginine-rich (SR)-like protein family that regulates alternative splicing of numerous genes in a concentration-dependent manner. Several types of cancer cells up-regulate Tra2β expression, while the regulatory mechanism of Tra2β expression remains to be elucidated. In this study, we examined the transcriptional regulation and possible functions of Tra2β in human colon cancer cells. We cloned 959 bp-upstream of the human TRA2β 5'-flank into luciferase constructs. Chromatin immunoprecipitation (ChIP) was employed to identify crucial cis element(s) and trans activator(s) of the TRA2β promoter. Tra2β expression in the human colon and colon cancer tissues was examined by immunohistochemistry. In response to sodium arsenite, colon cancer cells (HCT116) increased levels of TRA2β1 mRNA encoding a functional, full-length Tra2β with a peak around 6 h without changing its mRNA stability. Transient expression assays using a reporter gene driven by serially truncated TRA2β promoters and Chip assay demonstrated that an Ets1-binding site present at -64 to -55 bp was crucial for basal transcription, while three heat shock elements (HSEs) located at -145 to -99 bp mediated the oxidant-induced transactivation of TRA2β. Tra2β knockdown caused apoptosis of HCT116 cells. Tra2β were preferentially expressed in proliferative compartment of normal human colonic glands and adenocarcinomas, where Ets1 and heat shock factor 1 were also highly expressed. Our results suggest that oxidative stress-responsive Tra2β may play an important role in colon cancer growth.
(キーワード): Adenocarcinoma / アポトーシス (apoptosis) / Arsenites / Base Sequence / Colonic Neoplasms / DNA-Binding Proteins / Gene Expression Regulation, Neoplastic / Gene Knockdown Techniques / Heat-Shock Response / Humans / Molecular Sequence Data / Neoplasm Proteins / Nerve Tissue Proteins / 酸化ストレス (oxidative stress) / Promoter Regions, Genetic / Proto-Oncogene Protein c-ets-1 / RNA, Messenger / RNA, Neoplasm / RNA-Binding Proteins / Sodium Compounds / Transcription Factors / Transcription, Genetic / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00535-012-0745-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23361474; ● Summary page in Scopus @ Elsevier: 2-s2.0-84889888934

(DOI: 10.1007/s00535-012-0745-2, PubMed: 23361474, Elsevier: Scopus) Manami Honda, Yuki Kuwano, Sakurako Katsuura-Kamano, Kinuyo Fujita, Yoko Akaike, Shizuka Kano, Kensei Nishida, Kiyoshi Masuda and Kazuhito Rokutan :
Chronic academic stress increases a group of microRNAs in peripheral blood,
PLoS ONE, Vol.8, No.10, e75960, 2013.

(要約): MicroRNAs (miRNAs) play key roles in regulation of cellular processes in response to changes in environment. In this study, we examined alterations in miRNA profiles in peripheral blood from 25 male medical students two months and two days before the National Examination for Medical Practitioners. Blood obtained one month after the examination were used as baseline controls. Levels of seven miRNAs (miR-16, -20b, -26b, -29a, -126, -144 and -144*) were significantly elevated during the pre-examination period in association with significant down-regulation of their target mRNAs (WNT4, CCM2, MAK, and FGFR1 mRNAs) two days before the examination. State anxiety assessed two months before the examination was positively and negatively correlated with miR-16 and its target WNT4 mRNA levels, respectively. Fold changes in miR-16 levels from two days before to one month after the examination were inversely correlated with those in WNT4 mRNA levels over the same time points. We also confirmed the interaction between miR-16 and WNT4 3'UTR in HEK293T cells overexpressing FLAG-tagged WNT4 3'UTR and miR-16. Thus, a distinct group of miRNAs in periheral blood may participate in the integrated response to chronic academic stress in healthy young men.
(キーワード): Adult / Carrier Proteins / Humans / Male / MicroRNAs / Protein-Serine-Threonine Kinases / Receptor, Fibroblast Growth Factor, Type 1 / Stress, Psychological / Teaching / Wnt4 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0075960
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24130753; ● Search Scopus @ Elsevier (PMID): 24130753; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0075960

(DOI: 10.1371/journal.pone.0075960, PubMed: 24130753) Kiyoshi Masuda, Yuki Kuwano, Kensei Nishida, Kazuhito Rokutan and Issei Imoto :
NF90 in Posttranscriptional Gene Regulation and MicroRNA Biogenesis.,
International Journal of Molecular Sciences, Vol.14, No.8, 17111-17121, 2013.

(要約): Gene expression patterns are effectively regulated by turnover and translation regulatory (TTR) RNA-binding proteins (RBPs). The TTR-RBPs control gene expression at posttranscriptional levels, such as pre-mRNA splicing, mRNA cytoplasmic export, turnover, storage, and translation. Double-stranded RNA binding proteins (DSRBPs) are known to regulate many processes of cellular metabolism, including transcriptional control, translational control, mRNA processing and localization. Nuclear factor 90 (NF90), one of the DSRBPs, is abundantly expressed in vertebrate tissue and participates in many aspects of RNA metabolism. NF90 was originally purified as a component of a DNA binding complex which binds to the antigen recognition response element 2 in the interleukin 2 promoter. Recent studies have provided us with interesting insights into its possible physiological roles in RNA metabolism, including transcription, degradation, and translation. In addition, it was shown that NF90 regulates microRNA expression. In this review, we try to focus on the function of NF90 in posttranscriptional gene regulation and microRNA biogenesis.
(キーワード): Animals / Gene Expression Regulation, Neoplastic / Humans / MicroRNAs / Neoplasms / Nuclear Factor 90 Proteins / Protein Biosynthesis / RNA Interference / RNA Stability / RNA, Messenger
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/ijms140817111
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23965975; ● Summary page in Scopus @ Elsevier: 2-s2.0-84883187751

(DOI: 10.3390/ijms140817111, PubMed: 23965975, Elsevier: Scopus) Naoko Yamagishi, Shigetada Kondo, Kiyoshi Masuda, Kensei Nishida, Yuki Kuwano, Duyen T Dang, Long H Dang, Takeshi Nikawa and Kazuhito Rokutan :
Chronic inhibition of tumor cell-derived VEGF enhances the malignant phenotype of colorectal cancer cells,
BMC Cancer, Vol.13, 229, 2013.

(要約): Vascular endothelial growth factor-a (VEGF)-targeted therapies have become an important treatment for a number of human malignancies. The VEGF inhibitors are actually effective in several types of cancers, however, the benefits are transiently, and the vast majority of patients who initially respond to the therapies will develop resistance. One of possible mechanisms for the acquired resistance may be the direct effect(s) of VEGF inhibitors on tumor cells expressing VEGF receptors (VEGFR). Thus, we investigated here the direct effect of chronic VEGF inhibition on phenotype changes in human colorectal cancer (CRC) cells. To chronically inhibit cancer cell-derived VEGF, human CRC cell lines (HCT116 and RKO) were chronically exposed (2 months) to an anti-VEGF monoclonal antibody (mAb) or were disrupted the Vegf gene (VEGF-KO). Effects of VEGF family members were blocked by treatment with a VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI). Hypoxia-induced apoptosis under VEGF inhibited conditions was measured by TUNEL assay. Spheroid formation ability was assessed using a 3-D spheroid cell culture system. Chronic inhibition of secreted/extracellular VEGF by an anti-VEGF mAb redundantly increased VEGF family member (PlGF, VEGFR1 and VEGFR2), induced a resistance to hypoxia-induced apoptosis, and increased spheroid formation ability. This apoptotic resistance was partially abrogated by a VEGFR-TKI, which blocked the compensate pathway consisted of VEGF family members, or by knockdown of Vegf mRNA, which inhibited intracellular function(s) of all Vegf gene products. Interestingly, chronic and complete depletion of all Vegf gene products by Vegf gene knockout further augmented these phenotypes in the compensate pathway-independent manner. These accelerated phenotypes were significantly suppressed by knockdown of hypoxia-inducible factor-1α that was up-regulated in the VEGF-KO cell lines. Our findings suggest that chronic inhibition of tumor cell-derived VEGF accelerates tumor cell malignant phenotypes.
(キーワード): 分散分析 (analysis of variance) / Antibodies, Monoclonal / アポトーシス (apoptosis) / Enzyme Inhibitors / Gene Knockdown Techniques / HCT116 Cells / Humans / Hypoxia-Inducible Factor 1 / Phenotype / Pregnancy Proteins / Spheroids, Cellular / Vascular Endothelial Growth Factor A / Vascular Endothelial Growth Factor Receptor-1 / Vascular Endothelial Growth Factor Receptor-2
(徳島大学機関リポジトリ): ● Metadata: 105896
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/1471-2407-13-229
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23651517; ● Summary page in Scopus @ Elsevier: 2-s2.0-84877039223

(徳島大学機関リポジトリ: 105896, DOI: 10.1186/1471-2407-13-229, PubMed: 23651517, Elsevier: Scopus) Kiyoshi Masuda, Yuki Kuwano, Kensei Nishida and Kazuhito Rokutan :
Application of DNA microarray technology to gerontological studies,
Methods in Molecular Biology, Vol.1048, 285-308, 2013.

(要約): Gene expression patterns change dramatically in aging and age-related events. The DNA microarray is now recognized as a useful device in molecular biology and widely used to identify the molecular mechanisms of aging and the biological effects of drugs for therapeutic purpose in age-related diseases. Recently, numerous technological advantages have led to the evolution of DNA microarrays and microarray-based techniques, revealing the genomic modification and all transcriptional activity. Here, we show the step-by-step methods currently used in our lab to handling the oligonucleotide microarray and miRNA microarray. Moreover, we introduce the protocols of ribonucleoprotein [RNP] immunoprecipitation followed by microarray analysis (RIP-chip) which reveal the target mRNA of age-related RNA-binding proteins.
(キーワード): Aging / Gene Expression / Humans / Immunoprecipitation / MicroRNAs / Oligonucleotide Array Sequence Analysis / RNA-Binding Proteins / Ribonucleoproteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/978-1-62703-556-9_19
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23929111; ● Summary page in Scopus @ Elsevier: 2-s2.0-84934438449

(DOI: 10.1007/978-1-62703-556-9_19, PubMed: 23929111, Elsevier: Scopus) Shizuka Kano, Kensei Nishida, Chihiro Nishiyama, Yoko Akaike, Keisuke Kajita, Ken Kurokawa, Kiyoshi Masuda, Yuki Kuwano, Toshihito Tanahashi and Kazuhito Rokutan :
Truncated serine/arginine-rich splicing factor 3 accelerates cell growth through up-regulating c-Jun expression,
The Journal of Medical Investigation : JMI, Vol.60, No.3-4, 228-235, 2013.

(要約): Serine/arginine-rich splicing factor 3 (SRSF3), a member of the SRSF family, plays a wide-ranging role in gene expression. The human SRSF3 gene generates a major mRNA isoform encoding a functional, full-length protein and a PTC-containing isoform (SRSF3-PTC). The latter is expected to be degraded through the nonsense-mediated mRNA decay system. However, it was reported that SRSF3-PTC mRNA was produced under stressful conditions and translated into a truncated SRSF3 protein (SRSF3-TR). To disclose unknown functions of SRSF3-TR, we established Flp-In-293 cells stably expressing SRSF3-TR. The SRSF3-TR-expressing cells increased mRNA and protein levels of positive regulators for G1 to S phase transition (cyclin D1, cyclin D3, CDC25A, and E2F1) and accelerated their growth. c-Jun is required for progression through the G1 phase, the mechanism by which involves transcriptional control of the cyclin D1 gene. We also found that the JUN promoter activity was significantly increased in the Flp-In-293 cells stably expressing SRSF3-TR, compared with mock-transfected control cells. The SRSF3-TR-expressing cells increased c-Jun and Sp-1 levels, which are important for the positive autoregulation and basal transcription of JUN, respectively. Our results suggest that stress-inducible SRSF3-TR may participate in the acceleration of cell growth through facilitating c-Jun-mediated G1 progression under stressful conditions.
(キーワード): Alternative Splicing / Base Sequence / Cell Line / Cell Proliferation / DNA / G1 Phase Cell Cycle Checkpoints / Genes, bcl-1 / Genes, jun / Humans / Molecular Sequence Data / Oxidative Stress / Peptide Fragments / Promoter Regions, Genetic / RNA-Binding Proteins / Up-Regulation
(徳島大学機関リポジトリ): ● Metadata: 106361
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.60.228
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24190040; ● Summary page in Scopus @ Elsevier: 2-s2.0-84887007242

(徳島大学機関リポジトリ: 106361, DOI: 10.2152/jmi.60.228, PubMed: 24190040, Elsevier: Scopus) Sakurako Katsuura, Yuki Kuwano, Naoko Yamagishi, Ken Kurokawa, Keisuke Kajita, Yoko Akaike, Kensei Nishida, Kiyoshi Masuda, Toshihito Tanahashi and Kazuhito Rokutan :
MicroRNAs miR-144/144* and miR-16 in peripheral blood are potential biomarkers for naturalistic stress in healthy Japanese medical students.,
Neuroscience Letters, Vol.516, No.1, 79-84, 2012.

(要約): Non-coding microRNAs (miRNAs) are suggested to serve fundamental roles in cellular stress responses and in coping with sudden environmental changes in experimental animals. We examined whether naturalistic stressor-responsive miRNAs were detectable in whole blood. Blood and saliva were collected between 16:00 and 17:00 from 10 healthy medical students (5 males and 5 females; aged 22.4±0.8 years, mean±SD) 7 weeks before, one day before, immediately after, and one week after a nationally administered examination for academic promotion. Samples obtained one week after the examination were used as baseline controls. State anxiety and salivary cortisol levels reached maximum levels the day before the examination. Eleven candidate miRNAs (miR-144, -144*, -16, -15a, -19a, -19b, -26b, -30b, -106b, -126, and -142-3p) were extracted using a human miRNA microarray, and quantitative real-time reverse transcription PCR confirmed significant elevation of miR-144/144* and miR-16 levels immediately after finishing the examination. miR-16 levels in individual students were positively correlated with those of serum tumor necrosis factor (TNF)- measured immediately after the examination. Percentage changes in miR-144* and miR-16 levels from immediately after to one week after the examination were significantly correlated with percentage changes in circulating interferon- and/or TNF- levels over the same time points. Our results suggest that miR-144/144* and miR-16 may constitute a part of an integrated response to naturalistic stressors in healthy young adults.
(キーワード): Biological Markers / Female / Humans / Interferon-gamma / 日本 (Japan) / Male / MicroRNAs / Prevalence / Stress, Psychological / Students, Medical / Tumor Necrosis Factor-alpha / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.neulet.2012.03.062
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22484483; ● Summary page in Scopus @ Elsevier: 2-s2.0-84860258035

(DOI: 10.1016/j.neulet.2012.03.062, PubMed: 22484483, Elsevier: Scopus) Ken Kurokawa, Toshihito Tanahashi, Tsutomu Iima, Yuta Yamamoto, Yoko Akaike, Kensei Nishida, Kiyoshi Masuda, Yuki Kuwano, Yoshiki Murakami, Masakazu Fukushima and Kazuhito Rokutan :
Role of miR-19b and its target mRNAs in 5-fluorouracil resistance in colon cancer cells.,
Journal of Gastroenterology, Vol.47, No.8, 883-895, 2012.

(要約): BACKGROUND: Drug resistance in colorectal cancers is assumed to be mediated by changes in the expression of microRNAs, but the specific identities and roles of microRNAs are largely unclear. We examined the effect of 5-fluorouracil (5-FU) resistance on microRNA expression. METHODS: Two types of 5-FU-resistant colon cancer cells were derived from the DLD-1 and KM12C cell lines. The expressions of microRNAs were profiled with a microarray containing 723 microRNAs and validated by quantitative real-time polymerase chain reaction (qRT-PCR). To survey the downstream mediators of microRNA, we used a microRNA:mRNA immunoprecipitation (RIP)-Chip and pathway analysis tool to identify potential direct targets of microRNA. RESULTS: In response to 5-FU, miR-19b and miR-21 were over-expressed in 5-FU-resistant cells. Of note, miR-19b was up-regulated 3.47-fold in the DLD-1 resistant cells, which exhibited no alteration in cell cycle profiles despite exposure to 5-FU. After transfection of miR-19b, specific mRNAs were recruited to microRNA:mRNA complexes isolated with Ago2 antibody and subjected to whole-genome transcriptional analysis. In this analysis, 66 target mRNAs were enriched by at least 5.0-fold in the microRNA:mRNA complexes from DLD-1 resistant cells. Ingenuity pathway analysis of mRNA targets significantly (P < 0.05) indicated the category "Cell Cycle" as a probable area of the molecular and cellular function related with 5-FU resistance. Among candidate mRNA targets, SFPQ and MYBL2 have been linked to cell cycle functions. CONCLUSIONS: We revealed up-regulation of miR-19b in response to 5-FU and potential targets of miR-19b mediating the cell cycle under treatment with 5-FU. Our study provides an important insight into the mechanism of 5-FU resistance in colorectal cancers.
(キーワード): Antimetabolites, Antineoplastic / Cell Line, Tumor / Colonic Neoplasms / Drug Resistance, Neoplasm / Fluorouracil / Gene Expression Regulation, Neoplastic / Humans / MicroRNAs / Microarray Analysis / RNA, Messenger / Real-Time Polymerase Chain Reaction / Transfection / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00535-012-0547-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22382630; ● Summary page in Scopus @ Elsevier: 2-s2.0-84867572383

(DOI: 10.1007/s00535-012-0547-6, PubMed: 22382630, Elsevier: Scopus) Kiyoshi Masuda, Yuki Kuwano, Kensei Nishida and Kazuhito Rokutan :
General RBP expression in human tissues as a function of age.,
Ageing Research Reviews, Vol.11, No.4, 423-431, 2012.

(要約): Gene expression patterns vary dramatically in a tissue-specific and age-dependent manner. RNA-binding proteins that regulate mRNA turnover and/or translation (TTR-RBPs) critically affect the subsets of expressed proteins. Although many proteins implicated in age-related processes are encoded by mRNAs that are targets of TTR-RBPs, very little is known regarding the tissue- and age-dependent expression of TTR-RBPs in humans. Recent analysis of TTR-RBPs expression using human tissue microarray has provided us interesting insight into their possibly physiologic roles as a function of age. This analysis has also revealed striking discrepancies between the levels of TTR-RBPs in senescent human diploid fibroblasts (HDFs), widely used as an in vitro model of aging, and the levels of TTR-RBPs in tissues from individuals of advancing age. In this article, we will review our knowledge of human TTR-RBP expression in different tissues as a function of age.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.arr.2012.01.005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22326651; ● Summary page in Scopus @ Elsevier: 2-s2.0-84866507457

(DOI: 10.1016/j.arr.2012.01.005, PubMed: 22326651, Elsevier: Scopus) Yoko Akaike, Ken Kurokawa, Keisuke Kajita, Yuki Kuwano, Kiyoshi Masuda, Kensei Nishida, Seung Kang Wan, Toshihito Tanahashi and Kazuhito Rokutan :
Skipping of an alternative intron in the srsf1 3' untranslated region increases transcript stability.,
The Journal of Medical Investigation : JMI, Vol.58, No.3-4, 180-187, 2011.

(要約): The srsf1 gene encodes serine/arginine-rich splicing factor 1 (SRSF1) that participates in both constitutive and alternative splicing reactions. This gene possesses two ultraconserved elements in the 3' untranslated region (UTR). Skipping of an alternative intron between the two elements has no effect on the protein-coding sequence, but it generates a premature stop codon (PTC)-containing mRNA isoform, whose degradation is considered to depend on nonsense-mediated mRNA decay (NMD). However, several cell lines (HCT116, RKO, HeLa, and WI38 cells) constitutively expressed significant amounts of the srsf1 PTC variant. HCT116 cells expressed the PTC variant nearly equivalent to the major isoform that includes the alternative intron in the 3' UTR. Inhibition of NMD by silencing a key effecter UPF1 or by treatment with cycloheximide failed to increase amounts of the PTC variant in HCT116 cells, and the PTC variant was rather more stable than the major isoform in the presence of actinomycin D. Our results suggest that the original stop codon may escape from the NMD surveillance even in skipping of the alternative intron. The srsf1 gene may produce an alternative splice variant having truncated 3' UTR to relief the microRNA- and/or RNA-binding protein-mediated control of translation or degradation. J. Med. Invest. 58: 180-187, August, 2011.
(徳島大学機関リポジトリ): ● Metadata: 83832
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.58.180
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21921418; ● Search Scopus @ Elsevier (PMID): 21921418; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.180

(徳島大学機関リポジトリ: 83832, DOI: 10.2152/jmi.58.180, PubMed: 21921418) Sakurako Katsuura, Yoshiko Kamezaki, Naoko Yamagishi, Yuki Kuwano, Kensei Nishida, Kiyoshi Masuda, Toshihito Tanahashi, Tomoko Kawai, Kokichi Arisawa and Kazuhito Rokutan :
Circulating vascular endothelial growth factor is independently and negatively associated with trait anxiety and depressive mood in healthy Japanese university students.,
International Journal of Psychophysiology, Vol.81, No.1, 38-43, 2011.

(要約): Anxiety and depressive mood are sometimes accompanied by modulation of neuroendocrine and immune functions. The aim of this study was to identify circulating immune mediators reflecting anxiety and depressive mood in healthy young adults. Anxiety and depressive mood in 209 healthy medical students (125 males and 84 females, aged 20.7±2.7years (mean±SD)) were assessed by the Spielberger state-trait anxiety inventory (STAI) and the Zung self-rating depression scale (Zung-SDS), respectively. Cortisol and chromogranin A (CgA) levels in saliva were measured using enzyme immunoassay kits, and 50 different mediators in sera were measured by a multiplex-suspension array system. The level of statistical significance was set at =0.05. Forty-four mediators were measurable in sera, and each mediator showed substantial individual variations. After determining Pearson correlation coefficients, we selected candidate cytokines whose levels were associated with STAI-state (2 cytokines), STAI-trait (8 cytokines), or SDS scores (8 cytokines). The candidate cytokines plus interleukin (IL)-1, IL-6, tumor necrosis factor-, and macrophage migration inhibitory factor were then subjected to multiple regression analysis adjusted for gender, BMI, and salivary concentrations of cortisol and CgA. Vascular endothelial growth factor (VEGF) was independently and negatively associated with both trait anxiety (p<0.05) and depressive mood (p<0.01). IL-1 showed independently positive association with depressive mood (p<0.05). Interactions between these two cytokines and gender or BMI were not observed. Besides IL-1, circulating VEGF may be a potential biomarker for negative mood states in healthy young adults.
(キーワード): Adolescent / Anxiety / Body Mass Index / 細胞質分裂 (cytokinesis) / Depressive Disorder / Endothelial Growth Factors / 女性 (female) / Humans / Hydrocortisone / 日本 (Japan) / 男性 (male) / Psychiatric Status Rating Scales / Questionnaires / Regression Analysis / Saliva / Sex Factors / Students / Universities / Vascular Endothelial Growth Factor A / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ijpsycho.2011.04.004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21545819; ● Summary page in Scopus @ Elsevier: 2-s2.0-79957757010

(DOI: 10.1016/j.ijpsycho.2011.04.004, PubMed: 21545819, Elsevier: Scopus) Ken Kurokawa, Toshihito Tanahashi, Akiho Murata, Yoko Akaike, Sakurako Katsuura, Kensei Nishida, Kiyoshi Masuda, Yuki Kuwano, Tomoko Kawai and Kazuhito Rokutan :
Effects of chronic academic stress on mental state and expression of glucocorticoid receptor α and β isoforms in healthy Japanese medical students.,
Stress, Vol.14, No.4, 431-438, 2011.

(要約): Chronic academic stress responses were assessed by measuring mental state, salivary cortisol levels, and the glucocorticoid receptor (GR) gene expression in healthy Japanese medical students challenging the national medical license examination. Mental states of 17 male and 9 female medical undergraduates, aged 25.0 ± 1.2 years (mean ± SD), were assessed by the State and Trait Anxiety Inventory (STAI) and the Self-Rating Depression Scale (SDS) 2 months before, 2 days before, and 1 month after the examination. At the same time points, saliva and blood were collected. STAI-state scores peaked 2 days before the examination. Scores on STAI-trait and SDS, and salivary cortisol levels were consistently higher during the pre-examination period. One month after the examination, all these measures had significantly decreased to baseline levels. Real-time reverse transcription PCR showed that this chronic anxious state did not change the expression of the functional GRα mRNA isoform in peripheral leukocytes, while it resulted in reduced expression of the GRβ isoform 2 days before the examination. Our results replicate and extend a significant impact of chronic academic stressors on the mental state of healthy Japanese medical students and suggest a possible association of GRβ gene in response to psychological stress.
(キーワード): Adult / Asian Continental Ancestry Group / Female / Humans / Hydrocortisone / Male / Protein Isoforms / RNA, Messenger / Receptors, Glucocorticoid / 唾液腺 (salivary glands) / Stress, Psychological / Students, Medical
(出版サイトへのリンク): ● Publication site (DOI): 10.3109/10253890.2011.555930
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21438768; ● Search Scopus @ Elsevier (PMID): 21438768; ● Search Scopus @ Elsevier (DOI): 10.3109/10253890.2011.555930

(DOI: 10.3109/10253890.2011.555930, PubMed: 21438768) Yongsheng Shi, Kensei Nishida, Dafne Di Giammartino Campigli and James L. Manley :
Heat shock-induced SRSF10 dephosphorylation displays thermotolerance mediated by Hsp27.,
Molecular and Cellular Biology, Vol.31, No.3, 458-465, 2010.

(要約): Gene regulation in response to environmental stress is critical for the survival of all organisms. From Saccharomyces cerevisiae to humans, it has been observed that splicing of mRNA precursors is repressed upon heat shock. However, a mild heat pretreatment often prevents splicing inhibition in response to a subsequent and more severe heat shock, a phenomenon called splicing thermotolerance. We have shown previously that the splicing regulator SRSF10 (formerly SRp38) is specifically dephosphorylated by the phosphatase PP1 in response to heat shock and that dephosphorylated SRSF10 is responsible for splicing repression caused by heat shock. Here we report that a mild heat shock protects SRSF10 from dephosphorylation during a second and more severe heat shock. Furthermore, this "thermotolerance" of SRSF10 phosphorylation, like that of splicing, requires de novo protein synthesis, specifically the synthesis of heat shock proteins. Indeed, overexpression of one of these proteins, Hsp27, inhibits SRSF10 dephosphorylation in response to heat shock and does so by interaction with SRSF10. Our data thus provide evidence that splicing thermotolerance is acquired through maintenance of SRSF10 phosphorylation and that this is mediated at least in part by Hsp27.
(キーワード): Adaptation, Physiological / Cell Cycle Proteins / Cell Nucleus / HSP27 Heat-Shock Proteins / Heat-Shock Response / Hela Cells / Humans / Neoplasm Proteins / Phosphorylation / Protein Binding / Protein Biosynthesis / Protein Transport / RNA-Binding Proteins / Recombinant Proteins / Repressor Proteins / Temperature
(出版サイトへのリンク): ● Publication site (DOI): 10.1128/MCB.01123-10
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21135127; ● Search Scopus @ Elsevier (PMID): 21135127; ● Search Scopus @ Elsevier (DOI): 10.1128/MCB.01123-10

(DOI: 10.1128/MCB.01123-10, PubMed: 21135127) Kiyoshi Masuda, Shigetada Teshima-Kondo, Mina Mukaijo, Naoko Yamagishi, Yoshiko Nishikawa, Kensei Nishida, Tomoko Kawai and Kazuhito Rokutan :
A novel tumor-promoting function residing in the 5' non-coding region of vascular endothelial growth factor mRNA.,
PLoS Medicine, Vol.5, No.5, e94, 2008.

(要約): BACKGROUND: Vascular endothelial growth factor-A (VEGF) is one of the key regulators of tumor development, hence it is considered to be an important therapeutic target for cancer treatment. However, clinical trials have suggested that anti-VEGF monotherapy was less effective than standard chemotherapy. On the basis of the evidence, we hypothesized that vegf mRNA may have unrecognized function(s) in cancer cells. METHODS AND FINDINGS: Knockdown of VEGF with vegf-targeting small-interfering (si) RNAs increased susceptibility of human colon cancer cell line (HCT116) to apoptosis caused with 5-fluorouracil, etoposide, or doxorubicin. Recombinant human VEGF165 did not completely inhibit this apoptosis. Conversely, overexpression of VEGF165 increased resistance to anti-cancer drug-induced apoptosis, while an anti-VEGF165-neutralizing antibody did not completely block the resistance. We prepared plasmids encoding full-length vegf mRNA with mutation of signal sequence, vegf mRNAs lacking untranslated regions (UTRs), or mutated 5'UTRs. Using these plasmids, we revealed that the 5'UTR of vegf mRNA possessed anti-apoptotic activity. The 5'UTR-mediated activity was not affected by a protein synthesis inhibitor, cycloheximide. We established HCT116 clones stably expressing either the vegf 5'UTR or the mutated 5'UTR. The clones expressing the 5'UTR, but not the mutated one, showed increased anchorage-independent growth in vitro and formed progressive tumors when implanted in athymic nude mice. Microarray and quantitative real-time PCR analyses indicated that the vegf 5'UTR-expressing tumors had up-regulated anti-apoptotic genes, multidrug-resistant genes, and growth-promoting genes, while pro-apoptotic genes were down-regulated. Notably, expression of signal transducers and activators of transcription 1 (STAT1) was markedly repressed in the 5'UTR-expressing tumors, resulting in down-regulation of a STAT1-responsive cluster of genes (43 genes). As a result, the tumors did not respond to interferon (IFN)alpha therapy at all. We showed that stable silencing of endogenous vegf mRNA in HCT116 cells enhanced both STAT1 expression and IFNalpha responses. CONCLUSIONS: These findings suggest that cancer cells have a survival system that is regulated by vegf mRNA and imply that both vegf mRNA and its protein may synergistically promote the malignancy of tumor cells. Therefore, combination of anti-vegf transcript strategies, such as siRNA-based gene silencing, with anti-VEGF antibody treatment may improve anti-cancer therapies that target VEGF.
(キーワード): 5' Untranslated Regions / Animals / Antineoplastic Agents / アポトーシス (apoptosis) / Cell Line, Tumor / Gene Expression Regulation, Neoplastic / Humans / Interferon-alpha / Mice / Neoplasm Transplantation / Neoplasms / RNA, Messenger / RNA, Small Interfering / STAT1 Transcription Factor / 血管内皮増殖因子 (vascular endothelial growth factor)
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pmed.0050094
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18494554; ● Summary page in Scopus @ Elsevier: 2-s2.0-44449097601

(DOI: 10.1371/journal.pmed.0050094, PubMed: 18494554, Elsevier: Scopus) Tomoko Kawai, Kyoko Morita, Kiyoshi Masuda, Kensei Nishida, Michiyo Shikishima, Masayuki Ohta, Toshiro Saito and Kazuhito Rokutan :
Gene expression signature in peripheral blood cells from medical students exposed to chronic psychological stress.,
Biological Psychology, Vol.76, No.3, 147-155, 2007.

(要約): To assess response to chronic psychological stress, gene expression profiles in peripheral blood from 18 medical students confronting license examination were analyzed using an original microarray. Total RNA was collected from each subject 9 months before the examination and mixed to be used as a universal control. At that time, most students had normal scores on the state-trait anxiety inventory (STAI). However, STAI scores were significantly elevated at 2 months and at 2 days before the examination. Pattern of the gene expression profile was more uniform 2 days before than 2 months before the examination. We identified 24 genes that significantly and uniformly changed from the universal control 2 days before the examination. Of the 24 genes, real-time PCR validated changes in mRNA levels of 10 (PLCB2, CSF3R, ARHGEF1, DPYD, CTNNB1, PPP3CA, POLM, IRF3, TP53, and CCNI). The identified genes may be useful to assess chronic psychological stress response.
(キーワード): Adaptation, Psychological / Adult / Anxiety / Blood Cells / Cluster Analysis / 女性 (female) / Gene Expression Profiling / Gene Expression Regulation / Humans / 男性 (male) / Oligonucleotide Array Sequence Analysis / Personality Inventory / Stress, Psychological / Students, Medical
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopsycho.2007.07.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17766027; ● Summary page in Scopus @ Elsevier: 2-s2.0-35348916170

(DOI: 10.1016/j.biopsycho.2007.07.008, PubMed: 17766027, Elsevier: Scopus) Tomoko Kawai, Kyoko Morita, Kiyoshi Masuda, Kensei Nishida, Atsuo Sekiyama, Shigetada Kondo, Masayuki Ohta, Toshiro Saito and Kazuhito Rokutan :
Physical exercise-associated gene expression signatures in peripheral blood.,
Clinical Journal of Sport Medicine, Vol.17, No.5, 375-383, 2007.

(要約): To assess response to physical stress, gene expression profiles in peripheral blood cells were analyzed using an original microarray carrying 1467 stress-responsive complementary DNA probes. Gene expression was analyzed at 4, 24, and 48 hours after exercising on a cycle ergometer at 60% VO2 max for 1 hour (aerobic exercise) or until exhausted (exhaustive exercise). Institute of Health Biosciences, University of Tokushima Graduate School. Twelve healthy male students of the postgraduate or undergraduate school. The volunteers performed the aerobic or exhaustive exercise on a cycle ergometer. Detection of aerobic exercise-responsive or exhaustive exercise-responsive genes in peripheral blood cells. Aerobic and exhaustive exercise transiently changed the expression of 21 and 16 genes, respectively, with the peak at 4 hours. Only 2 genes significantly responded to both types of exercise. Exhaustive but not aerobic exercise produced a secondary response with significantly altered expression of 14 genes at 24 hours. Five of those genes encode receptors for neurotransmitters (HTR1A, CHRNB2, GABRB3, GABRG3, and LOC51289). The behavior of the individual genes shown here may be informative to objectively assess acute physical stress and exhaustion-associated responses.
(キーワード): Adaptation, Physiological / Adult / Blood Cells / Ergometry / Exercise / 遺伝子発現 (gene expression) / Humans / 男性 (male) / Oligonucleotide Array Sequence Analysis / Prospective Studies / RNA, Messenger / Time Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1097/JSM.0b013e31814c3e4f
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17873550; ● Summary page in Scopus @ Elsevier: 2-s2.0-34548693648

(DOI: 10.1097/JSM.0b013e31814c3e4f, PubMed: 17873550, Elsevier: Scopus)

MISC

六反一仁, 桑野由紀, 西田憲生, 増田清士 :
ストレス脆弱性のゲノミクス，エピジェネティクス,
ストレス科学, Vol.26, No.4, 357-364, 2012年.

(キーワード): ストレス / 発達 / 遺伝子-環境相互作用 / 脆弱性遺伝子 / エピジェネティクス / Stress / Development / Gene-environment interactions / Vulnerability genes / Epigenetics
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520290885101169792

(CiNii: 1520290885101169792) 桑野由紀, 本田真奈美, 西田憲生, 増田清士, 六反一仁 :
遺伝子発現からみたストレス脆弱性,
ストレス科学, Vol.26, No.4, 384-394, 2012年.

(キーワード): ストレス / 遺伝子発現 / 末梢白血球 / マイクロRNA / Stress / Gene expression / Peripheral blood leukocytes / MicroRNAs
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520009410125272064

(CiNii: 1520009410125272064) Norihiro Kubota, Shuichi Suzuki, Yuki Kuwano, Sayaka Kakiyama, Naomi Harima-Mizusawa and Kensei Nishida :
IDO1 and FOXP3: Possible immune-regulating genes alleviating cedar pollinosis via L. plantarum YIT 0132.,
Allergy, Vol.79, No.7, 1966-1969, 2024.

(キーワード): Humans / Indoleamine-Pyrrole 2,3,-Dioxygenase / Rhinitis, Allergic, Seasonal / Forkhead Transcription Factors / Cryptomeria / Pollen
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/all.16039
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38279616; ● Summary page in Scopus @ Elsevier: 2-s2.0-85183620025

(DOI: 10.1111/all.16039, PubMed: 38279616, Elsevier: Scopus)

総説・解説

西田憲生, 桑野由紀, 六反一仁 :
プロバイオティクスによる新しい健康長寿戦略脳腸相関を介した睡眠改善作用,
ストレス科学, Vol.34, No.4, 230-239, 2020年6月.

(キーワード): 脳腸相関 / 腸内細菌 / プロバイオティクス / 概日リズム / 睡眠
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520009410124394112

(CiNii: 1520009410124394112) Kensei Nishida, Yuki Kuwano, Tatsuya Nishikawa, Kiyoshi Masuda and Kazuhito Rokutan :
RNA Binding Proteins and Genome Integrity.,
International Journal of Molecular Sciences, Vol.18, No.7, Jun. 2017.

(要約): Genome integrity can be threatened by various endogenous or exogenous events. To counteract these stressors, the DNA damage response network contributes to the prevention and/or repair of genomic DNA damage and serves an essential function in cellular survival. DNA binding proteins are involved in this network. Recently, several RNA-binding proteins (RBPs) that are recruited to DNA damage sites have been shown to be direct players in the prevention or repair of DNA damage. In addition, non-coding RNAs, themselves, are involved in the RNA-mediated DNA repair system. Furthermore, RNA modification such as m6A methylation might also contribute to the ultraviolet-responsive DNA damage response. Accumulating evidence suggests that RNA metabolism is more deeply involved in diverse cellular functions than previously expected, and is also intricately associated with the maintenance of genome integrity. In this review, we highlight the roles of RBPs in the maintenance of genome integrity.
(キーワード): Animals / Cell Nucleus / DNA Damage / DNA Repair / Genome / Humans / RNA Processing, Post-Transcriptional / RNA, Untranslated / RNA-Binding Proteins / Telomere Shortening
(徳島大学機関リポジトリ): ● Metadata: 112411
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/ijms18071341
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28644387; ● Search Scopus @ Elsevier (PMID): 28644387; ● Search Scopus @ Elsevier (DOI): 10.3390/ijms18071341

(徳島大学機関リポジトリ: 112411, DOI: 10.3390/ijms18071341, PubMed: 28644387) 六反一仁, 西田憲生, 桑野由紀 :
腸に定着してストレスを緩和する乳酸菌,
FOOD Style 21, Vol.21, No.6, 29-31, 2016年6月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522543655944080896

(CiNii: 1522543655944080896) 西田憲生, 桑野由紀, 六反一仁 :
エピジェネティクス・NMD,
Journal of Gastrointestinal Research, Vol.24, No.4, 288-291, 2016年. 田中裕基, 桑野由紀, 西川達哉, 西田憲生, 六反一仁 :
末梢血の遺伝子発現解析によるストレス評価,
ストレス科学, Vol.30, No.4, 285-289, 2016年. 西田憲生, 桑野由紀, 成戸卓也, 六反一仁 :
ストレスとエピジェネテイクス,
産業精神保健, Vol.23, No.3, 234-238, 2015年3月. 六反一仁, 桑野由紀, 西田憲生, 増田清士 :
ストレスバイオマーカーの同定と今後の展開,
Surgery Frontier, Vol.20, No.4, 413-418, 2013年. 六反一仁, 桑野由紀, 増田清士, 西田憲生, 神尾陽子 :
ASDに特徴的な末梢血白血球の遺伝子発現,
精神経誌, SS470-SS474, 2012年. Dafne Giammartino Campigli Di, Kensei Nishida and James L. Manley :
Mechanisms and consequences of alternative polyadenylation.,
Molecular Cell, Vol.43, No.6, 853-866, Sep. 2011.

(要約): Alternative polyadenylation (APA) is emerging as a widespread mechanism used to control gene expression. Like alternative splicing, usage of alternative poly(A) sites allows a single gene to encode multiple mRNA transcripts. In some cases, this changes the mRNA coding potential; in other cases, the code remains unchanged but the 3' UTR length is altered, influencing the fate of mRNAs in several ways, for example, by altering the availability of RNA binding protein sites and microRNA binding sites. The mechanisms governing both global and gene-specific APA are only starting to be deciphered. Here we review what is known about these mechanisms and the functional consequences of alternative polyadenylation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.molcel.2011.08.017
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21925375; ● Search Scopus @ Elsevier (PMID): 21925375; ● Search Scopus @ Elsevier (DOI): 10.1016/j.molcel.2011.08.017

(DOI: 10.1016/j.molcel.2011.08.017, PubMed: 21925375)

講演・発表

Kensei Nishida :
The Gut-Brain Axis: Probiotics and their Impact on Health, Unveiling effects on Sleep Improvement and Stress Alleviation.,
14TH (INDIA) PROBIOTIC SYMPOSIUM, Thiruvananthapuram, INDIA, 2024, Feb. 2024. Yasushi Sato, Kazuyoshi Noda, Yasuyuki Okada, Kensei Nishida, Yutaka Kawano, Toshihito Tanahashi, Masanori Takehara, Yasuteru Fujino, Koichi Okamoto, Hiroshi Miyamoto and Tetsuji Takayama :
Exosomal miR-199a-3p secreted from cancer-associated adipocytes promote pancreatic cancer progression.,
DDW2023, Chicago, May 2023. Yuki Kuwano, Kensei Nishida, 佐竹譲 and Kazuhito Rokutan :
Nuclear retention of transcribed ultraconserved region uc.138 promotes colon cancer cell growth,
Cell Symposium-Regulatory RNAs, Berlin, Germany, May 2019. Kensei Nishida :
Health Benefits: Probiotics and the gut-brain axis: effects on physical and mental symptoms of stress,
IDF WDS Daejeon 2018, Oct. 2018. Saijo Saka, Kensei Nishida, Tatsuya Nishikawa, Yuki Kuwano and Kazuhito Rokutan :
A novel role of serine/arginine-rich splicing factor 7 in cell cycle progression,
KEYSTONE SYMPOSIA on Molecular and Cellular Biology, Banff, Alberta, Canada, Feb. 2017. Yuki Kuwano, Satake Yuzuru, Tatsuya Nishikawa, Fujita Kinuyo, Saijo Saki, Kensei Nishida and Kazuhito Rokutan :
Ultraconserved region-containing Transformer 2-beta4 associates with nucleolin and regulates cellular proliferation,
KEYSTONE SYMPOSIA on Molecular and Cellular Biology, Banff, Alberta, Canada, Feb. 2017. Kazuhito Rokutan, Kensei Nishida, Yuki Kuwano, Daisuke Sawada and Shigeru Fujiwara :
Enteric-colonizing Lactobacillus gasseri CP2305 improves stress-related adverse behaviours.,
Oct. 2016. Yuki Kuwano, K kajita, S Kano, Y Satake, M Fujita, M Itai, Kensei Nishida and Kazuhito Rokutan :
Ultraconserved region-containing transformer 24 inhibits senesces of colon cancer cells.,
Cell symposia-Human genomics, Singapore, Nov. 2015. Shizuka Kano, Kensei Nishida, Yuki Kuwano, Takuya Naruto and Kazuhito Rokutan :
Analysis of functional transcribed-ultraconserved regions in SR protein family.,
Cold Spring Harbor Laboratory Meeting on Eukaryotic mRNA processing., Sep. 2015. Saki Saijo, Kensei Nishida, Shizuka Kano, Takuya Naruto, Yuki Kuwano and Kazuhito Rokutan :
A role of serine/arginine-rich splicing factor 7 in cell cycle progression,
Cold Spring Harbor Laboratory Meeting on Eukaryotic mRNA processing, Aug. 2015. Kensei Nishida, Saki Saijo, Shizuka Kano, Takuya Naruto, Yuki Kuwano and Kazuhito Rokutan :
Analysis of 3 end processing factors expression during epithelial-mesenchymal transition,
Cold Spring Harbor Laboratory Meeting on Eukaryotic mRNA processing, Aug. 2015. Yuki Kuwano, Y Satake, S Kano, K Fujita, M Itai, Kensei Nishida, Takuya Naruto, Kiyoshi Masuda and Kazuhito Rokutan :
Transformer 2 and miR-204 regulate cell death through competitive binding to 3 UTR of BCL2 mRNA,
Cell Symposia Regulatory RNAs, San Francisco, Oct. 2014. S Kano, Kensei Nishida, Y Satake, K Fujita, M Itai, Takuya Naruto, Kiyoshi Masuda, Yuki Kuwano and Kazuhito Rokutan :
Analysis of function transcribed ultraconserved regions of SR protein family,
Cell Symposia Regulatory RNAs, San Francisco, Oct. 2014. Shizuka Kano, Kensei Nishida, Yuzuru Satake, Yoko Akaike, Kinuyo Fujita, Kiyoshi Masuda, Yuki Kuwano and Kazuhito Rokutan :
Arsenite stress-inducible truncated serine/arginine-rich splicing factor 3 regulates interleukin-8 in human colon cancer cells,
The 5th EMBO Meeting 2013, Amsterdam, Sep. 2013. Yoko Akaike, Kiyoshi Masuda, Yuzuru Satake, Kinuyo Fujita, Shizuka Kano, Kensei Nishida, Yuki Kuwano and Kazuhito Rokutan :
Homeodomain interacting protein kinase 2 regulates interaction between heterochromatin protein 1 gamma and trimethylated histone H3 Lys9,
The 5th EMBO Meeting 2013, Amsterdam, Sep. 2013. Kinue Fujita, Yuki Kuwano, Shizuka Kano, Yuzuru Satake, Kensei Nishida, Kiyoshi Masuda and Kazuhito Rokutan :
Socioeconomic status-related gene expression profiles in peripheral leukocytes from medical staffs,
The international conference on social stratification and health, Tokyo, Sep. 2013. Kiyoshi Masuda, Y Akaike, K Fujita, M Honda, Y Satake, K Kajita, Kensei Nishida, Yuki Kuwano and Kazuhito Rokutan :
Hu antigen R (HuR) Regulates an Alternative Splicing of Transformer 2-beta (Tra2beta) and Induces lncRNA (Tra2beta4) under Oxidative Stress,
Cell Symposia Regulatory RNAs, Sitges, Spain, Dec. 2012. Yuki Kuwano, K. Kajita, Y. Satake, Y. Akaike, M. Honda, F. Fujita, Kensei Nishida, Kiyoshi Masuda and Kazuhito Rokutan :
The RNA binding protein Transformer-2 beta modulates processing of microRNAs,
Cell symposia-Functional RNAs, Dec. 2012. Y Akaike, Kiyoshi Masuda, K Fujita, M Honda, Y Satake, K Kajita, Kensei Nishida, Yuki Kuwano and Kazuhito Rokutan :
Hu antigen R (HuR) Functions as An Alternative Splicing Regulator of Transformer 2-beta (TRA2beta) in response to Oxidative Stress,
4th EMBO meeting 2012, Niece, Sep. 2012. K Kajita, Yuki Kuwano, Y Satake, Y Akaike, M Honda, K Fujita, Kensei Nishida, Kiyoshi Masuda and Kazuhito Rokutan :
Ultraconserved element-containing Transformer 24 mRNA regulates cellular senescence,
The 4th EMBO Meeting 2012, Niece, Sep. 2012. Yuki Kuwano, Keisuke Kajita, Yuzuru Satake, Ken Kurokawa, Naoko Yamagishi, Yoko Akaike, Manami Honda, Kensei Nishida, Kiyoshi Masuda, Toshihito Tanahashi and Kazuhito Rokutan :
Transfomer-2beta regulates apoptosis through post-transcriptional regulation of bcl-2,
Cell Symposia Regulatory RNAs, Chicago, Oct. 2011. Kiyoshi Masuda, Naoko Yamagishi, Ken Kurokawa, Yuzuru Satake, Keisuke Kajita, Yoko Akaike, Manami Honda, Kensei Nishida, Yuki Kuwano, Toshihito Tanahashi and Kazuhito Rokutan :
Hu antigen R (huR) functions as an alternative pre-mRNA splicing enhancer of transformer 2-beta (Tra2beta) on exon definition under oxidative stress,
Cell Symposia Regulatory RNAs, Chicago, Oct. 2011. Ken Kurokawa, Yoko Akaike, Keisuke Kajita, Naoko Yamagishi, Yuzuru Satake, Manami Honda, Kensei Nishida, Yuki Kuwano, Kiyoshi Masuda, Toshihito Tanahashi and Kazuhito Rokutan :
Serine/arginine-rich splicing factor 3 (SRSF3) regulates G1/S checkpoint and p53-dependent apoptosis,
3rd EMBO Meeting 2011, Wien, Sep. 2011. Manami Honda, Sakurako Katsuura, Yuki Kuwano, Naoko Yamagishi, Ken Kurokawa, Yuzuru Satake, Keisuke Kajita, Yoko Akaike, Kensei Nishida, Kiyoshi Masuda, Toshihito Tanahashi and Kazuhito Rokutan :
High-throughput screening of immunomodulators identifies VEGF as a potential biomarker for trait anxiety and depressive mood in healthy Japanese university students,
The International Conference on Social Stratification and Health 2011, Tokyo, Aug. 2011. 桑野由紀, Nazere Keyoumu, 西田憲生, 森野豊之 :
抗老化RNA uc.138 のm6Aメチル化修飾を介した大腸がん悪性化メカニズム,
第46回日本分子生物学会年会, 2023年12月. 西田憲生 :
月経前症状と腸内細菌-プロバイオティクスによる症状緩和の可能性-,
第38回日本女性医学学会学術集会，徳島，2023, 2023年12月. 西田憲生, 常山幸一, 赤池雅史 :
医学科1年次における垂直統合型の早期体験実習の試み,
第55回日本医学教育学会大会, 2023年7月. 山内翔葵, 宮本亮介, 武藤浩平, 桑野由紀, Nazere Keyoumu, 西田憲生, 橘このか, 和泉唯信, 森野豊之 :
表現型に基づく優先順位付けを用いたALSの病的バリアント検索,
第64回日本神経学会学術大会, 2023年6月. 平尾章博, 佐藤康史, 田中宏典, 田中貴大, 友成哲, 谷口達哉, 岡本耕一, 六車直樹, 西田憲生, 高山哲治 :
肝細胞癌においてmiR-125b-5pは上皮間葉転換を引き起こし，ソラフェニブに対して耐性を獲得する,
第19回日本臨床腫瘍学会学術集会, 2022年2月. 桑野由紀, 西田憲生, 森野豊之 :
RNA修飾を介した大腸がん細胞の抗老化スイッチの解明,
第44回日本分子生物学会年会, 2021年12月. 西田憲生, 清水真祐子, 吾妻雅彦, 常山幸一, 赤池雅史 :
オンラインPBLチュートリアルの実施から見えてきた課題,
第53回日本医学教育学会大会, 2021年7月. 西田憲生 :
プロバイオティクスの秘めたる可能性∼睡眠の質的改善作用∼,
1. 第43回日本生物学的精神医学会・第51回日本神経精神薬理学会合同年会, 2021年7月. 西田憲生, 清水真祐子, 常山幸一, 赤池雅史 :
オンラインPBLチュートリアルの実施報告ならびにその効果と課題,
大学教育カンファレンスin徳島, 2021年1月. 桑野由紀, 西田憲生, 六反一仁 :
大腸がん細胞に高発現する機能性RNA uc.138による大腸がん悪性化メカニズムの解明,
第43回日本分子生物学会年会, 2020年12月. 西田憲生 :
腸内細菌と睡眠:プロバイオティクスの脳腸相関を介した新しい機能,
第29回腸内フローラシンポジウム, 2020年11月. 桑野由紀, 西田憲生, 六反一仁 :
超保存領域を内在するT-UCRのRNAメチル化を介した大腸がん悪性化機構,
第42回日本分子生物学会年会, 2019年12月. 西田憲生, 田中裕基, 桑野由紀, 六反一仁 :
大腸がん細胞の遊走能獲得を制御するmicroRNAの探索,
第61回日本消化器病学会大会, 2019年11月. 西田憲生 :
脳と腸は腸内細菌によって操られている? ∼ストレスと脳腸相関:プロバイオティクスによるストレス緩和作用∼,
第40回健康づくり提唱のつどい, 2019年7月. 三好人正, 村山典聡, 中川忠彦, 岡本耕一, 佐藤康史, 六車直樹, 西田憲生, 常山幸一, 藤盛孝博, 高山哲治 :
直腸NETのmiRNA-Gene-Pathwayを介した転移機序の解明とmiR-144-3p/451aの転移予測マーカーとしての意義.,
第15回日本消化管学会総会学術集会, 2019年2月. 桑野由紀, 西川達哉, 西條早希, 西田憲生, 六反一仁 :
機能性RNA TRA2β4の核局在が誘導する大腸がん悪性化メカニズム,
第41回日本分子生物学会年会, 2018年11月. 西田憲生 :
脳腸相関を介したプロバイオティクスの身体症状緩和作用,
第3回生活習慣病予防のための機能性食品開発に関する研究会, 2017年12月. 西條早希, 西田憲生, 田中裕基, 板井美樹, 藤田絹代, 桑野由紀, 六反一仁 :
HOXA5遺伝子領域を含む新規転写産物の同定と機能解析,
第40回日本分子生物学会年会, 2017年12月. 田中裕基, 西田憲生, 西條早希, 板井美樹, 西川達哉, 桑野由紀, 六反一仁 :
大腸がん細胞の遊走能獲得過程におけるDNAメチル化修飾の役割,
第40回日本分子生物学会年会, 2017年12月. 桑野由紀, 山中佐織, 西川達哉, 佐竹譲, 藤田絹代, 西條早希, 田中裕基, 西田憲生, 六反一仁 :
TRA2β4のRNAメチル化を介した大腸癌悪性化の分子基盤,
第40回日本分子生物学会年会, 2017年12月. 西川達哉, 桑野由紀, 高原由実子, 西條早希, 田中裕基, 板井美樹, 西田憲生, 六反一仁 :
hnRNP familyを介した超保存領域を内在するTRA2β4 RNAの発現調節メカニズムの解明,
第40回日本分子生物学会年会, 2017年12月. 西田憲生, 田中裕基, 西條早希, 板井美樹, 西川達哉, 桑野由紀, 六反一仁 :
microRNA23b/27b/24 clusterを介した大腸がん細胞の形質転換制御機構,
第40回日本分子生物学会年会, 2017年12月. 藤野泰輝, 西田憲生, 高山哲治 :
microRNA arrayを用いた大腸SM癌リンパ節転移の網羅的解析.,
第25回日本消化器関連学会週間(JDDW2017), 2017年10月. 西川達哉, 桑野由紀, 小玉美幸, 西條早希, 田中裕基, 板井美樹, 藤田絹代, 西田憲生, 六反一仁 :
Ultraconserved regionを内在するTRA2β4の発現制御と大腸がんの細胞増殖メカニズムの解明,
第39回日本分子生物学会年会, 2016年12月. 桑野由紀, 西田憲生, 西川達哉, 六反一仁 :
Serine/arginine-richスプライシング因子SRSFを介したエピジェネティック調節機構,
第39回日本分子生物学会年会, 2016年11月. 西田憲生 :
ストレスと脳腸相関:プロバイオティクスによるストレス緩和作用,
第25回腸内フローラシンポジウム, 2016年11月. 西田憲生 :
脳腸相関を介したプロバイオティクスのストレス緩和作用,
第8回ヤクルト代田カンファレンス, 2016年11月. 西田憲生 :
脳腸相関をターゲットとした創薬に向けて,
新薬理学セミナー2016(プロバイオティクスが拓く新たな創薬研究), 2016年7月. 西田憲生 :
脳腸相関を介して作用するプロバイオティクスの可能性,
第89回日本産業衛生学会, 2016年5月. 西條早希, 西田憲生, 狩野静香, 田中裕基, 桑野由紀, 六反一仁 :
大腸がん細胞におけるSRSF7を介した新規細胞増殖機構,
第102回日本消化器病学会総会, 2016年4月. Kensei Nishida, Akito Kato-kataoka, Mai Takada, Takahiro Matsuki, Mitsuhisa Kawai, Kouji Miyazaki, Hiroki Tanaka, Yuki Kuwano and Kazuhito Rokutan :
Fermented milk containing Lactobacillus casei Shirota prevents onset of physical symptoms under stress condition,
Physiological Sciences, 93rd Annual Meeting, Mar. 2016. 西田憲生, 狩野静香, 佐竹謙, 板井美樹, 田中裕基, 桑野由紀, 六反一仁 :
EMTmicroRNA,
第12回日本消化管学会総会学術集会, 2016年2月. 西田憲生, 狩野静香, 佐竹謙, 板井美樹, 田中裕基, 桑野由紀, 六反一仁 :
上皮間葉移行モデルを用いたEMT関連microRNAの探索,
第12回日本消化管学会総会学術集会, 2016年2月. 小玉美幸, 桑野由紀, 佐竹譲, 狩野静香, 藤田絹代, 板井美樹, 西田憲生, 六反一仁 :
Ultraconserved regionを内在するTRA2β4を介した細胞周期調節メカニズムの解析,
第38回日本分子生物学会年会, 2015年12月. 西條早希, 西田憲生, 狩野静香, 佐竹謙, 藤田絹代, 板井美樹, 田中裕基, 桑野由紀, 六反一仁 :
大腸がん細胞におけるSRSF7を介した細胞周期調節機能の解析,
第38回日本分子生物学会年会, 2015年12月. 佐竹譲, 桑野由紀, 狩野静香, 藤田絹代, 板井美樹, 田中裕基, 西田憲生, 六反一仁 :
TRA2β4とnucleolinの相互作用を介した大腸癌細胞増殖メカニズムの解明,
第38回日本分子生物学会年会, 2015年12月. 高田麻衣, 加藤豪人, 河合光久, 権藤祐輔, 宮崎幸司, 西田憲生, 六反一仁 :
L.,
第31回日本ストレス学会学術総会, 2015年11月. 藤田絹代, 桑野由紀, 千葉美穂, 西田憲生, 六反一仁 :
医療従事者の不安・うつ状態を反映する末梢血マイクロRNAの検索,
第31回日本ストレス学会学術総会, 2015年11月. 桑野由紀, 佐竹譲, 狩野静香, 藤田絹代, 西田憲生, 六反一仁 :
新規非コードRNA TRA2β4を介した大腸がん悪性化の分子基盤,
第10回臨床ストレス応答学会, 2015年11月. 狩野静香, 西田憲生, 桑野由紀, 成戸卓也, 佐竹謙, 板井美樹, 藤田絹代, 六反一仁 :
Serin/Arginine-rich splicing factor 3(SRSF3)のがん悪性化メカニズムの解明,
第37回日本分子生物学会年会, 2014年11月. 桑野由紀, 藤田絹代, 狩野静香, 佐竹譲, 西田憲生, 六反一仁 :
自閉症スペクトラム障害に特徴的な末梢血のマイクロRNA発現パターンの検討,
第30回日本ストレス学会学術総会, 2014年11月. 西田憲生, 狩野静香, 板井美樹, 藤田絹代, 佐竹譲, 成戸卓也, 桑野由紀, 六反一仁 :
上皮間葉移行モデルの構築とメカニズム解析,
第9回臨床ストレス応答学会, 2014年11月. 桑野由紀, 梶田敬介, 佐竹譲, 狩野静香, 藤田絹代, 板井美樹, 西田憲生, 成戸卓也, 六反一仁 :
非コードRNA(T-UCR)を介した大腸がんの細胞増殖メカニズムの検討,
第9回臨床ストレス応答学会, 2014年11月. 増田清士, 西田憲生, 六反一仁, 井本逸勢 :
RNA結合蛋白質による転写後調節機構の異常と消化器がん発症機構の解明,
第 100 回日本消化器病学会総会, 2014年4月. 西田憲生, 狩野静香, 桑野由紀, 六反一仁 :
スプライシング調節因子SRSF3の新規炎症メディエーターとしての機能解析,
第10回日本消化管学会総会学術集会, 2014年2月. 藤田絹代, 桑野由紀, 赤池瑤子, 狩野静香, 佐竹譲, 西田憲生, 富士翔子, 酒巻咲子, 安原由子, 谷岡哲也, 六反一仁 :
社会格差の視点からみた精神的健康と影響因子-医療従事者の場合-,
第37回中国・四国精神保健学会, 2013年12月. 増田清士, 赤池瑶子, 庄田勝俊, 村田知慧, 田嶋敦, 桑野由紀, 西田憲生, 六反一仁, 井本逸勢 :
HuR stimulates cell growth in colon cancer cells by regulating alternative splicing under oxidative stress,
第36回日本分子生物学会年会, 2013年12月. 増田清士, 西田憲生, 六反一仁, 井本逸勢 :
新規RNA結合蛋白質による食堂扁平上皮がんの発がん機構の解明,
第100回日本消化器病学会四国支部例会, 2013年11月. 西田憲生, 赤池瑶子, 増田清士, 佐竹譲, 藤田絹代, 狩野静香, 桑野由紀, 六反一仁 :
Homeodomain interacting protein kinase 2 (HIPK2)は，クロマチン構成因子heterochromatin protein 1γ (HP1γ) をリン酸化し，トリメチル化ヒストンH3 Lys9への結合を阻害する,
第8回臨床ストレス応答学会大会, 2013年11月. 狩野静香, 西田憲生, 赤池瑶子, 藤田絹代, 佐竹譲, 桑野由紀, 六反一仁 :
酸化ストレス下におけるtruncated SRSF3タンパク質のインターロイキン8発現調節機構,
第8回臨床ストレス応答学会, 2013年11月. 藤田絹代, 桑野由紀, 西田憲生, 赤池瑶子, 狩野静香, 六反一仁 :
医療従事者を対象とした社会格差による健康障害メカニズムの検討,
第29回日本ストレス学会学術総会, 2013年11月. 宮原圭吾, 桑野由紀, 西田憲生, 赤池瑶子, 狩野静香, 六反一仁 :
ストレス応答性Transformer 2β遺伝子の発現を介した細胞増殖の調節メカニズム,
第29回日本ストレス学会学術総会, 2013年11月. 増田清士, 赤池瑶子, 庄田勝俊, 村田知慧, 桑野由紀, 西田憲生, 田嶋敦, 井本逸勢 :
RNA結合蛋白質HuRによる選択的スプライシング制御機構の解明,
第29回日本ストレス学会学術総会, 2013年11月. 増田清士, 西田憲生, 六反一仁, 井本逸勢 :
選択的スプライシング制御因子SRSF3による大腸がん細胞の悪性形質変化誘導の解明,
第21回日本消化器関連学会週間, 2013年10月. 桑野由紀, 本田真奈美, 梶田敬介, 赤池瑶子, 藤田絹代, 佐竹譲, 西田憲生, 増田清士, 六反一仁 :
ヒト末梢血における慢性心理的ストレス応答性マイクロRNAの同定,
Neuro 2013, 2013年6月. S Kano, 西田憲生, 桑野由紀, 増田清士, K Kurokawa, 六反一仁 :
Ultraconserved exon-containing SRSF3 mRNA isoform is specifically translated to the truncated SRSF3protein under oxidative stress,
第35回日本分子生物学会, 2012年12月. 赤池瑶子, 増田清士, 黒川憲, 佐竹譲, 梶田敬介, 本田真奈美, 藤田絹代, 西田憲生, 桑野由紀, 六反一仁 :
HIPK2はクロマチン構成因子HP1γと相互作用しDNA修復を制御する,
第35回日本分子生物学会, 2012年12月. 西田憲生, 本田真奈美, 桑野由紀, 藤田絹代, 梶田敬介, 赤池瑶子, 増田清士, 六反一仁 :
健常大学生の医師国家試験ストレスに応答する末梢血マイクロRNAの検索,
第28回日本ストレス学会学術総会, 2012年12月. 赤池瑶子, 増田清士, 黒川憲, 佐竹譲, 梶田敬介, 本田真奈美, 藤田絹代, 西田憲生, 桑野由紀, 六反一仁 :
HIPK2はクロマチン構成因子HP1γと相互作用しDNA修復を制御する,
第7回臨床ストレス応答学会大会, 2012年11月. 本田真奈美, 桑野由紀, 佐竹譲, 梶田敬介, 赤池瑶子, 藤田絹代, 西田憲生, 増田清士, 六反一仁 :
精神的ストレスに応答するヒト末梢血マイクロRNAの発現,
第7回臨床ストレス応答学会大会, 2012年11月. 桑野由紀, 梶田敬介, 佐竹譲, 赤池瑶子, 本田真奈美, 藤田絹代, 西田憲生, 増田清士, 六反一仁 :
選択的スプライシング因子Tra2βを介したBcl-2の転写後調節,
第7回臨床ストレス応答学会大会, 2012年11月. 西田憲生, 増田清士, 桑野由紀, 黒川憲, 狩野静香, 六反一仁 :
酸化ストレス下特異的に誘導されるtruncated SRSF3 proteinの新規機能解析,
第20回日本消化器関連学会週間, 2012年10月. 増田清士, 西田憲生, 六反一仁 :
酸化ストレスにおける選択的スプライシング制御異常と消化器がん発症機構の解明,
第20回日本消化器関連学会週間, 2012年10月. 赤池瑶子, 増田清士, 山岸直子, 黒川憲, 佐竹譲, 梶田敬介, 本田真奈美, 西田憲生, 桑野由紀, 六反一仁 :
酸化ストレス下での，HuRによるtransformer 2-beta (Tra2β)の選択的スプライシング制御機構,
第97回日本消化器病学会四国支部例会, 2012年6月. 増田清士, 神田瑞希, 赤池瑶子, 本田真奈美, 梶田敬介, 佐竹譲, 黒川憲, 山岸直子, 西田憲生, 桑野由紀, 六反一仁 :
アドリアマイシンによる，選択的スプライシング制御を介した新たな腫瘍抑制分子機構,
第97回日本消化器病学会四国支部例会, 2012年6月. 赤池瑶子, 増田清士, 山岸直子, 黒川憲, 佐竹譲, 梶田敬介, 本田真奈美, 西田憲生, 桑野由紀, 棚橋俊仁, 六反一仁 :
Hu antigen R (HuR) Functions as An Alternative Pre-mRNA Splicing Regulator of Transformer 2-beta (Tra2beta) under Oxidative Stress,
第34回日本分子生物学会年会, 2011年12月. 山岸直子, 近藤茂忠, 増田清士, 桑野由紀, 西田憲生, 六反一仁 :
VEGF遺伝子にコードされた腫瘍促進性non-coding RNAの発現制御機構,
第34回日本分子生物学会年会, 2011年12月. 本田真奈美, 桑野由紀, 山岸直子, 黒川憲, 佐竹譲, 梶田敬介, 赤池瑶子, 西田憲生, 増田清士, 棚橋俊仁, 六反一仁 :
精神的ストレスに応答するヒト末梢血マイクロRNAの発現,
第27回日本ストレス学会学術総会, 2011年11月. 梶田敬介, 桑野由紀, 山岸直子, 黒川憲, 佐竹譲, 赤池瑶子, 本田真奈美, 西田憲生, 増田清士, 棚橋俊仁, 六反一仁 :
酸化ストレス応答性Tra2beta4 mRNAによる細胞老化の制御,
第6回臨床ストレス応答学会大会, 2011年11月. 赤池瑶子, 増田清士, 山岸直子, 黒川憲, 佐竹譲, 梶田敬介, 本田真奈美, 西田憲生, 桑野由紀, 六反一仁 :
酸化ストレス下でのHuRによるtransformer 2-beta (Tra2beta)の選択的スプライシング制御機構,
第6回臨床ストレス応答学会大会, 2011年11月.

研究会・報告書: 西田憲生, 西條早希, 桑野由紀, 六反一仁 :
HOX遺伝子座の新規長鎖ノンコーディングRNAは大腸癌細胞の増殖を促進する,
第19回生体機能研究会, 2020年9月. 桑野由紀, 西川達哉, 西田憲生, 六反一仁 :
超保存領域を内在するT-UCRのRNAメチル化を介した大腸がん悪性化機構,
第18回生体機能研究会, 2019年7月. 西川達哉, 桑野由紀, 西田憲生, 六反一仁 :
hnRNP familyを介したTRA2B遺伝子の発現調節機構の解明,
第17回生体機能研究会, 2018年7月. 桑野由紀, 西川達哉, 西田憲生, 六反一仁 :
TRA2B遺伝子にコードされる超保存領域を介した大腸がん悪性化機構の解明,
第17回生体機能研究会, 2018年7月. 西田憲生, 桑野由紀, 西川達哉, 六反一仁 :
脳腸相関を介したプロバイオティクスのストレス緩和作用,
第17回生体機能研究会, 2018年7月. 西田憲生, 桑野由紀, 西川達哉, 六反一仁 :
microRNA23b/27b/24 cluster を介した大腸がん細胞の形質転換制御機構,
第16回生体機能研究会, 2017年9月. 桑野由紀, 西川達哉, 西田憲生, 六反一仁 :
超保存領域をコードするTRA2β4のRNA修飾を介した大腸がん悪性化機構,
第16回生体機能研究会, 2017年9月. 西川達哉, 桑野由紀, 西田憲生, 六反一仁 :
hnRNP family を介したUltraconserved region を内在するTRA2B 遺伝子の発現調節機構の解明,
第16回生体機能研究会, 2017年9月. 西田憲生 :
食品による睡眠改善効果に関する検討,
第21回睡眠科学研究講座, 2017年6月. 田中裕基, 西田憲生, 板井美樹, 西條早希, 佐竹謙, 藤田絹代, 西川達哉, 桑野由紀, 六反一仁 :
大腸がん細胞の上皮間葉移行におけるDNAメチル化の網羅的解析,
第39回日本分子生物学会年会, 2016年11月. 西條早希, 西田憲生, 田中裕基, 板井美樹, 藤田絹代, 西川達哉, 桑野由紀, 六反一仁 :
SRSF7を介した細胞増殖調節メカニズムの解明,
第39回日本分子生物学会年会, 2016年11月. 西田憲生, 桑野由紀, 西條早希, 藤田絹代, 田中裕基, 板井美樹, 西川達哉, 六反一仁 :
乳酸菌L.カゼイ・シロタ株はストレスによる身体症状を緩和する,
第15回生体機能研究会, 2016年7月. 西條早希, 西田憲生, 西川達哉, 藤田絹代, 田中裕基, 板井美樹, 西川達哉, 六反一仁 :
大腸がん細胞におけるserine/arginine-rich splicing factor 7を介した新規細胞増殖機構の解明,
第15回生体機能研究会, 2016年7月. 桑野由紀, 佐竹謙, 藤田絹代, 西條早希, 西川達哉, 西田憲生, 六反一仁 :
新規非コードRNA TRA2β4を介した細胞周期調節メカニズムの解明,
第15回生体機能研究会, 2016年7月. 西田憲生, 加藤豪人, 松木隆広, 河合光久, 宮崎幸司, 田中裕基, 桑野由紀, 六反一仁 :
学術試験に伴う体調不良に対するL.カゼイ・シロタ株含有飲料の有効性の検討,
第93回日本生理学会大会, 2016年3月. Yuki Kuwano, Manami Honda, Kinuyo Fujita, Yoko Akaike, Shizuka Kano, Yuzuru Satake, Kensei Nishida and Kazuhito Rokutan :
Chronic academic stress increases a group of microRNAs in peripheral blood in healthy Japanese students.,
The international conference on social stratification and health 2013, Sep. 2013. 赤池瑶子, 増田清士, 佐竹譲, 藤田絹代, 狩野静香, 西田憲生, 桑野由紀, 六反一仁 :
Homeodomain interacting protein Kinase 2 (HIPK2) はクロマチン構成因子heterochromatin protein 1γ (HP1γ)をリン酸化し，トリメチル化ヒストンH3 Lys9 への結合を阻害する,
第12回生体機能研究会, 2013年7月. 桑野由紀, 梶田敬介, 佐竹譲, 赤池瑶子, 狩野静香, 藤田絹代, 西田憲生, 増田清士, 六反一仁 :
Transformer 2β RNA プロセシングを介した大腸がん悪性化の分子機構,
第12回生体機能研究会, 2013年7月.

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補助金・競争的資金: 超保存領域が内包する大腸がん発症リスクの分子メカニズムの解明 (研究課題/領域番号: 20K08309 )
mRNAプロセシングを介したがんのヘテロジェナイティの新規メカニズムの解明 (研究課題/領域番号: 16K09314 )
選択的ポリアデニレーション制御を介した新規大腸癌悪性形質獲得のメカニズムの解明 (研究課題/領域番号: 26860509 )
選択的ポリアデニレーションを介した新たな発癌機構の解明 (研究課題/領域番号: 24790705 )
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2024年12月23日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [医療管理学、医療系社会学 (Healthcare management
medical sociology)]
ライフサイエンス (Life sciences) [分子生物学 (Molecular biology)]
ライフサイエンス (Life sciences) [内科学一般 (Internal medicine - General)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
ライフサイエンス (Life sciences) [生理学 (Physiology)]
所属学会・所属協会: 日本ストレス学会
臨床ストレス応答学会
財団法人日本消化器病学会
日本消化管学会
日本医学教育学会
委員歴・役員歴: 日本ストレス学会 (評議員 [2015年11月〜2028年11月])
臨床ストレス応答学会 (評議員 [2013年11月〜2025年3月])
財団法人日本消化器病学会 (四国支部評議員 [2018年1月〜2025年3月])
日本消化管学会 (代議員 [2019年2月〜2025年2月])
日本医学教育学会 (代議員 [2023年8月〜2027年8月])
受賞: 2013年4月, 共通教育賞 (全学共通教育センター)
2019年2月, Best Teacher of the Year 2018 (医学部)
2020年3月, 医学部優秀教育賞 (共通)
2020年5月, 令和2年度日本栄養・食糧学会技術賞受賞
2020年6月, 学部長特別表彰 (徳島大学)
2023年3月, Best Teacher of the year 2022 (医学部)
活動: 医学部教育主任教員 (2013年3月〜2023年3月)
医学部教育支援センター副センター長 (2019年11月〜2023年3月)
FD委員会委員 (2020年4月〜2022年3月)
プログラム評価委員会委員 (2020年4月〜2022年3月)
教務委員会委員 (2020年4月〜2023年3月)
徳島大学教育研究ジャーナル編集委員 (2020年4月〜2023年3月)
カリキュラム評価委員会委員 (2020年4月〜2023年3月)
CBT統括責任者 (2020年4月〜2023年3月)
学生・教職員専門委員会 (2020年4月〜2023年3月)

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Jグローバル最終確認日: 2024/12/21 01:25
氏名（漢字）: 西田憲生
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氏名（英字）: Nishida Kensei
所属機関: 徳島大学准教授

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researchmap最終確認日: 2024/12/22 01:48
氏名（漢字）: 西田憲生
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更新日時: 2024/7/17 14:29
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所属: 徳島大学
部署: 大学院医歯薬学研究部
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研究者番号: 10624033

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 准教授

所属（過去の研究課題 情報に基づく）*注記: 2020/4/1 – 2022/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 准教授
2018/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 准教授
2016/4/1 – 2017/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 准教授
2015/4/1 : 徳島大学, 大学院医歯薬学研究部, 准教授
2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 准教授
2012/4/1 – 2013/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 助教

審査区分/研究分野: 研究代表者

生物系 / 医歯薬学 / 内科系臨床医学 / 消化器内科学
小区分53010:消化器内科学関連

キーワード: 研究代表者

ポリアデニレーション / ストレス / 発がんメカニズム / 選択的ポリアデニレーション / 発がん機構 / 発癌メカニズム / 選択的ポリアデニレーション制御 / 大腸癌 / ヘテロジェナイティ / 大腸がん / 上皮間葉移行 / RNAプロセシング / DNAメチル化 / マイクロRNA / microRNA / migration / DNA methylation / mRNAプロセシング / 超保存領域 / 腸管分化 / iPS細胞 / long non-coding RNA

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