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J-GLOBAL ID：202002263079455136   整理番号：20A2135357

SETD2はEZH2とAMPKシグナル伝達経路の統合により前立腺癌転移を制限する【JST・京大機械翻訳】

SETD2 Restricts Prostate Cancer Metastasis by Integrating EZH2 and AMPK Signaling Pathways

著者 (22件)： Yuan Huairui (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Han Ying (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Wang Xuege (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Li Ni (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Liu Qiuli (Department of Urology, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing 400042, China) ,  Yin Yuye (Department of Immunology, Key Laboratory of Immune Microenvironment and Diseases, NHC Key Laboratory of Antibody Technique, Department of Microbes and Infection, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jia...) ,  Wang Hanling (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Pan Lulu (State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China) ,  Li Li (State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai 200127, China) ,  Song Kun (State Key Laboratory of Oncogenes and Related Genes, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China) ,  Qiu Tong (Department of Obstetrics, Gynecology and Pediatrics, West China Second University Hospital, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Sichuan University, 20 Renmin South Road, Chengdu 610041, China) ,  Pan Qiang (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Chen Qilong (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Zhang Guoying (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Zang Yi (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Tan Minjia (State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China) ,  Zhang Jian (State Key Laboratory of Oncogenes and Related Genes, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China) ,  Li Qintong (Department of Obstetrics, Gynecology and Pediatrics, West China Second University Hospital, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education, Sichuan University, 20 Renmin South Road, Chengdu 610041, China) ,  Wang Xiaoming (Department of Immunology, Key Laboratory of Immune Microenvironment and Diseases, NHC Key Laboratory of Antibody Technique, Department of Microbes and Infection, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jia...) ,  Jiang Jun (Department of Urology, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing 400042, China) ,  Qin Jun (CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China) ,  Qin Jun (Department of Urology, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing 400042, China)
資料名： Cancer Cell  (Cancer Cell)
巻： 38  号： 3  ページ： 350-365.e7  発行年： 2020年 
JST資料番号： W1844A  ISSN： 1535-6108  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： オランダ (NLD)  言語： 英語 (EN)

抄録/ポイント： SETD2仲介H3K36me3のレベルはEZH2触媒H3K27me3と逆相関した。それにもかかわらず,これら2つの酵素活性が分子的に絡み合っているかどうかは不明である。ここでは,SETD2が,その基質EZH2を介し前立腺癌(PCa)転移を遅らせることを報告する。SETD2はEZH2分解を促進するEZH2をメチル化することを示した。SETD2欠損は,細胞が転移形質を獲得することを可能にするポリコーム抑制クロマチン状態を誘導する。逆に,非メチル化EZH2変異体またはEZH2への結合に欠損したSETD2変異体を有するマウスは,転移PCaを発現した。さらに,メトホルミン刺激AMPKシグナル伝達がFOXO3で収束してSETD2発現を刺激することを同定した。まとめると,著者らの結果は,SETD2-EZH2軸がPCa転移を制限するために代謝とエピジェネティックシグナル伝達を統合することを示す。Copyright 2020 Elsevier B.V., Amsterdam. All rights reserved. Translated from English into Japanese by JST.【JST・京大機械翻訳】

シソーラス用語： メチル化 ,  基質 ,  クロマチン ,  酵素活性度 ,  *前立腺 ,  *腫瘍転移 ,  *前立腺腫瘍 ,  *細胞情報伝達 ,  エピジェネティクス ,  脂肪族アミン
準シソーラス用語： 逆相関 ,  AMP活性化蛋白質キナーゼ ,  伝達経路 ,  *EZH2 , 【Automatic Indexing@JST】

著者キーワード (6件)： 前立腺癌転移 ,  エピジェネティックおよび代謝的調節不全 ,  SETD2 ,  EZH2 ,  AMPK ,  メトホルミン

分類 (2件)： 遺伝子発現  (EC02040Q) ,  抗腫よう薬の基礎研究  (GW16010A)

物質索引 (1件)： メトホルミン

タイトルに関連する用語 (6件)： EZH2 ,  AMPK ,  シグナル伝達経路 ,  統合 ,  前立腺癌 ,  制限