Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells

Yongmei Yang; Jie Du; Fen Liu; Xiaoyan Wang; Xiaohui Li; Yuanjian Li

doi:10.18632/oncotarget.19471

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Research Papers:

Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells

Yongmei Yang, Jie Du, Fen Liu, Xiaoyan Wang, Xiaohui Li and Yuanjian Li _

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Oncotarget. 2017; 8:59204-59216. https://doi.org/10.18632/oncotarget.19471

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Abstract

Yongmei Yang1,2, Jie Du1, Fen Liu3, Xiaoyan Wang3, Xiaohui Li1 and Yuanjian Li1

1Department of Pharmacology, Xiangya School of Pharmaceutical Science, Central South University, Changsha, China

2Department of Anatomy, School of Medicine, University of South China, Hengyang, China

3Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, China

Correspondence to:

Yuanjian Li, email: [email protected]

Xiaohui Li, email: [email protected]

Keywords: helicobacter pylori, caspase-3, E-cadherin, E-cadherin/carboxy-terminal fragment 3 (E-cad/CTF3), apoptosis

Received: January 04, 2017 Accepted: June 20, 2017 Published: July 22, 2017

ABSTRACT

This study was designed to investigate the role of caspase-3/E-cadherin in Helicobacter pylori (H. pylori) -induced gastric epithelial apoptosis in cells, animal models and clinical gastritis patients. In cultured gastric mucosal epithelial cells, gastric glandular epithelial cells and C57BL/6 mice, H. pylori infection significantly induced apoptosis of gastric epithelial cells, down-regulated full-length E-cadherin and Bcl-2 expression, and up-regulated cleaved-caspase-3, E-cadherin/carboxy-terminal fragment 3 and Bax expression. Z-DEVD-FMK, an inhibitor of caspase-3, attenuated the effect of H. pylori. E-cadherin overexpression significantly inhibited the apoptosis of GES-1 and SGC-7901 cells induced by the H. pylori. The results from clinical studies also showed down-regulation of E-cadherin, up-regulation of cleaved-caspase-3 expression and increased apoptosis in gastric tissues from gastritis patients with H. pylori infection. These results suggest that the caspase-3/E-cadherin pathway is involved in the apoptosis of gastric epithelial cells induced by H. pylori.

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Research Papers:

Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells

Abstract