Clinic of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke-University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
Exp Cell Res. 2009 Dec 10;315(20):3500-8. doi: 10.1016/j.yexcr.2009.07.029. Epub 2009 Aug 6.
Helicobacter pylori, a microaerophilic gram-negative bacterium, colonizes the human stomach. About 50% of the world's population is infected, and this infection is considered as the major risk factor for the development of gastric adenocarcinomas in 1% of infected subjects. Carcinogenesis is characterized by the process of epithelial-to-mesenchymal transition (EMT), in the course of which fully differentiated epithelial cells turn into depolarized and migratory cells. Concomitant disruption of adherence junctions (AJ) is facilitated by growth factors like hepatocyte growth factor 1 (HGF-1), but has been also shown to depend on ectodomain shedding of E-cadherin. The aim of this study was to investigate the impact of infection with H. pylori of NCI-N87 gastric epithelial cells on the shedding of E-cadherin and HGF-receptor c-Met. Our results show that infection with H. pylori provokes shedding of the surface proteins c-Met and E-cadherin. Evidence is provided that ADAM10 contributes to the shedding of c-Met and E-cadherin.
幽门螺杆菌（Helicobacter pylori）是一种微需氧革兰氏阴性菌，定植于人类胃部。约有 50%的世界人口受到感染，而这种感染被认为是导致 1%受感染者发展为胃腺癌的主要危险因素。癌变的特征是上皮-间充质转化（EMT）过程，在此过程中，完全分化的上皮细胞转变为去极化和迁移细胞。生长因子如肝细胞生长因子 1（HGF-1）有助于破坏黏附连接（AJ），但也已表明这依赖于 E-钙黏蛋白的外显子脱落。本研究旨在探讨幽门螺杆菌感染 NCI-N87 胃上皮细胞对 E-钙黏蛋白和 HGF 受体 c-Met 脱落的影响。我们的研究结果表明，幽门螺杆菌感染会引发表面蛋白 c-Met 和 E-钙黏蛋白的脱落。有证据表明 ADAM10 有助于 c-Met 和 E-钙黏蛋白的脱落。
