期刊
ONCOTARGET
卷 8, 期 35, 页码 59204-59216出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.19471
关键词
helicobacter pylori; caspase-3; E-cadherin; E-cadherin/carboxy-terminal fragment 3 (E-cad/CTF3); apoptosis
资金
- National Natural Science Foundation of China [81573486]
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/carboxyterminal 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 cleavedcaspase- 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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