中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
VPAC1 couples with TRPV4 channel to promote calcium-dependent gastric cancer progression via a novel autocrine mechanism

文献类型:期刊论文

作者Tang, Bo1,2; Wu, Jilin3,4; Zhu, Michael X.3,5; Sun, Xuemei2; Liu, Jingjing2; Xie, Rui2,6; Dong, Tobias Xiao1; Xiao, Yufeng2; Carethers, John M.7; Yang, Shiming2
刊名ONCOGENE
出版日期2019-05-16
卷号38期号:20页码:3946-3961
ISSN号0950-9232
DOI10.1038/s41388-019-0709-6
通讯作者Yang, Shiming(shimingyang@yahoo.com) ; Dong, Hui(h2dong@ucsd.edu)
英文摘要Although VPAC1 and its ligand vasoactive intestinal peptide (VIP) are important in gastrointestinal physiology, their involvements in progression of gastrointestinal tumor have not been explored. Here, we found that higher expression of VIP/VPAC1 was observed in gastric cancer compared to the adjacent normal tissues. The increased expression of VIP/VPAC1 in gastric cancer correlated positively with invasion, tumor stage, lymph node, distant metastases, and poor survival. Moreover, high expression of VIP and VPAC1, advanced tumor stage and distant metastasis were independent prognostic factors. VPAC1 activation by VIP markedly induced TRPV4-mediated Ca2+ entry, and eventually promoted gastric cancer progression in a Ca2+ signaling-dependent manner. Inhibition of VPAC1 and its signaling pathway could block the progressive responses. VPAC1/TRPV4/Ca2+ signaling in turn enhanced the expression and secretion of VIP in gastric cancer cells, enforcing a positive feedback regulation mechanism. Taken together, our study demonstrate that VPAC1 is significantly overexpressed in gastric cancer and VPAC1/TRPV4/Ca2+ signaling axis could enforce a positive feedback regulation in gastric cancer progression. VIP/VPAC1 may serve as potential prognostic markers and therapeutic targets for gastric cancer.
WOS关键词VASOACTIVE-INTESTINAL-PEPTIDE ; CELL-PROLIFERATION ; CA2+ ; VIP ; RECEPTOR ; ACTIVATION ; OVEREXPRESSION ; EXPRESSION ; SECRETION ; CATENIN
资助项目National Key Research and Development Program of China[2016YFC1302200] ; National Natural Science Foundation of China[81602577] ; Basic Science and Frontier Technology Research Project of Chongqing[cstc2017jcyjAX0149]
WOS研究方向Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
语种英语
WOS记录号WOS:000468035600013
出版者NATURE PUBLISHING GROUP
源URL[http://119.78.100.183/handle/2S10ELR8/289785]  
专题中国科学院上海药物研究所
通讯作者Yang, Shiming; Dong, Hui
作者单位1.Univ Calif San Diego, Sch Med, Dept Med, San Diego, CA 92103 USA
2.Third Mil Med Univ, Xinqiao Hosp, Dept Gastroenterol, Chongqing, Peoples R China
3.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai, Peoples R China
4.Univ Chinese Acad Sci, Beijing, Peoples R China
5.Univ Texas Hlth Sci Ctr Houston, McGovern Med Sch, Dept Integrat Biol & Pharmacol, Houston, TX 77030 USA
6.Zunyi Med Coll, Affiliated Hosp, Dept Gastroenterol, Zunyi, Peoples R China
7.Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA
推荐引用方式
GB/T 7714
Tang, Bo,Wu, Jilin,Zhu, Michael X.,et al. VPAC1 couples with TRPV4 channel to promote calcium-dependent gastric cancer progression via a novel autocrine mechanism[J]. ONCOGENE,2019,38(20):3946-3961.
APA Tang, Bo.,Wu, Jilin.,Zhu, Michael X..,Sun, Xuemei.,Liu, Jingjing.,...&Dong, Hui.(2019).VPAC1 couples with TRPV4 channel to promote calcium-dependent gastric cancer progression via a novel autocrine mechanism.ONCOGENE,38(20),3946-3961.
MLA Tang, Bo,et al."VPAC1 couples with TRPV4 channel to promote calcium-dependent gastric cancer progression via a novel autocrine mechanism".ONCOGENE 38.20(2019):3946-3961.

入库方式: OAI收割

来源:上海药物研究所

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