Gastrin acting on the cholecystokinin2 receptor induces cyclooxygenase-2 expression through JAK2/STAT3/PI3K/Akt pathway in human gastric cancer cells

被引：110

作者：

Xu, Wei ^{[1
]}

Chen, Guo-Sheng ^{[1
]}

Shao, Yun ^{[1
]}

Li, Xiao-Lin ^{[1
]}

Xu, Hai-Chen ^{[1
]}

Zhang, Hao ^{[1
]}

Zhu, Guo-Qing ^{[1
]}

Zhou, Yi-Chan ^{[1
]}

He, Xiao-Pu ^{[1
]}

Sun, Wei-Hao ^{[1
]}

机构：

[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Geriatr Gastroenterol, Nanjing 210029, Jiangsu, Peoples R China

来源：

CANCER LETTERS | 2013年 / 332卷 / 01期

关键词：

Gastric cancer; Cholecystokinin2; receptor; Cyclooxygenase-2; JAK2/STAT3; PI3K/Akt; HELICOBACTER-PYLORI INFECTION; EPITHELIAL-CELLS; COLORECTAL-CANCER; GENE-EXPRESSION; TUMOR-GROWTH; IN-VITRO; APOPTOSIS; PROLIFERATION; STAT3; ACTIVATION;

D O I：

10.1016/j.canlet.2012.12.030

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Gastrin, cholecystokinin2 receptor (CCK2R), and cyclooxygenase-2 (COX-2) have been implicated in the carcinogenesis and progression of gastric cancer. Our study demonstrated that antagonist or siRNA against CCK2R blocked amidated gastrin (G17)-induced activation of STAT3 and Akt in gastric cancer cell lines. G17-increased COX-2 expression and cell proliferation were effectively blocked by CCK2R antagonist and inhibitors of JAK2 and PI3K. In addition, knockdown of STAT3 expression significantly attenuated G17-induced PI3K/Akt activation, COX-2 expression, and cell proliferation. These results suggest that CCK2R-mediated COX-2 up-regulation via JAK2/STAT3/PI3K/Akt pathway is involved in the proliferative effect of G17 on human gastric cancer cells. (c) 2013 Elsevier Ireland Ltd. All rights reserved.

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页码：11 / 18

页数：8

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