CagA Associates with c-Met, E-Cadherin, and p120-Catenin in a Multiproteic Complex That Suppresses Helicobacter pylori–Induced Cell-Invasive Phenotype

摘要: Background. Helicobacter pylori induces an invasive phenotype in gastric epithelial cells through a mechanism that requires the type IV secretion system and phosphorylation of c-Met. The E-cadherin-catenin complex is major component adherens junctions functions as invasion suppressor. We investigated whether E-cadherin has role H. pylori-induced, c-Met phosphorylation- dependent cell-invasive phenotype. Methods. AGS lack are to stimulation were transduced with infected pylori. NCI-N87 cells, which endogenously express E-cadherin, also used for infection experiments. Results. was sufficient suppress not only pylori-mediated but p120-catenin tyrosine phosphorylation. led increased interactions between p120-catenin, p120-catenin. Using vitro assays, we showed CagA interacts Finally, using small interfering RNA, established c-Met. Conclusions. suggest alters complex, leading formation multiproteic composed CagA, c-Met, This abrogates suppresses induced by