Journal
EXPERIMENTAL CELL RESEARCH
Volume 315, Issue 20, Pages 3500-3508Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2009.07.029
Keywords
ADAM; Shedding; E-cadherin; c-Met; Gastric epithelial cell; NCI-N87
Categories
Funding
- Deutsche Forschungsgemeinschaft [GRK 1167/-1]
Ask authors/readers for more resources
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. (C) 2009 Published by Elsevier Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available