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J-GLOBAL ID：202202247364684201   整理番号：22A0451899

BPIFB1は鼻咽頭癌におけるGLUT1仲介H3K27アセチル化の下方制御を介して脈管形成擬態を阻害する【JST・京大機械翻訳】

BPIFB1 inhibits vasculogenic mimicry via downregulation of GLUT1-mediated H3K27 acetylation in nasopharyngeal carcinoma

著者 (28件)： Jiang Xianjie (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Jiang Xianjie (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Deng Xiangying (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Wang Jie (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Mo Yongzhen (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Shi Lei (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Shi Lei (Department of Oral and Maxillofacial Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China) ,  Wei Fang (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Zhang Shanshan (Department of Stomatology, Xiangya Hospital, Central South University, Changsha, Hunan, China) ,  Gong Zhaojian (Department of Oral and Maxillofacial Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China) ,  He Yi (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Xiong Fang (Department of Stomatology, Xiangya Hospital, Central South University, Changsha, Hunan, China) ,  Wang Yumin (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Guo Can (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Xiang Bo (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Xiang Bo (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Zhou Ming (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Zhou Ming (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Liao Qianjin (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Li Xiaoling (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Li Xiaoling (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Li Yong (Department of Medicine, Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA) ,  Li Guiyuan (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Li Guiyuan (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Xiong Wei (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Xiong Wei (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China) ,  Zeng Zhaoyang (NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China) ,  Zeng Zhaoyang (Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China)
資料名： Oncogene  (Oncogene)
巻： 41  号： 2  ページ： 233-245  発行年： 2022年 
JST資料番号： T0406A  ISSN： 0950-9232  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： ドイツ (DEU)  言語： 英語 (EN)

抄録/ポイント： 鼻咽頭癌(NPC)は,東南アジアと中国南部で有意な地域差と高い発生率を示す。殺細菌性/透過性増加-含有ファミリーBメンバー1(BPIFB1)は鼻咽頭上皮において比較的特異的で高度に発現する蛋白質である。BPIFB1発現はNPCで実質的にダウンレギュレートされ,NPC患者の予後不良と有意に関連している。しかし,BPIFB1がNPCを調節する特異的分子機構はよく理解されていない。この研究では,BPIFB1がNPCの代謝リプログラミングの調節により血管原性模倣を阻害することを見出した。BPIFB1はJNK/AP1シグナル伝達経路のダウンレギュレーションによりGLUT1転写を減少させた。変化した解糖はヒストンのアセチル化レベルを低下させ,血管原性模倣関連遺伝子,VEGFA,VE-カドヘリンおよびMMP2の発現を低下させ,最終的に血管原性模倣体の阻害をもたらす。著者らの知る限り,これはNPCにおける解糖と血管原性模倣の調節に関与する腫瘍抑制遺伝子としてのBPIFB1の役割と特異的機構に関する最初の報告である。全体として,これらの結果はNPC診断と治療のための新しい治療標的を提供する。Copyright The Author(s), under exclusive licence to Springer Nature Limited 2021 Translated from English into Japanese by JST.【JST・京大機械翻訳】

シソーラス用語： 血管 ,  *アセチル化 ,  遺伝子 ,  解糖 ,  上皮 ,  タンパク質 ,  ヒストン ,  *ダウンレギュレーション ,  癌抑制遺伝子 ,  カドヘリン ,  *GLUT1
準シソーラス用語： 予後不良 ,  分子機構 ,  リプログラミング ,  治療標的 , 【Automatic Indexing@JST】

分類 (3件)： 腫ようの化学・生化学・病理学  (GE02030N) ,  細胞生理一般  (EF02010S) ,  耳・鼻・咽頭・喉頭の腫よう  (GQ04000E)

タイトルに関連する用語 (8件)： 鼻咽頭癌 ,  GLUT1 ,  仲介 ,  アセチル化 ,  下方制御 ,  脈管形成 ,  擬態 ,  阻害