Helicobacter pylori induces cancer cell motility independent of the c-Met receptor.

ABSTRACT:

Background

The hepatocyte growth factor (HGF) receptor, c-Met, is strongly implicated in late-stage cancer progression and poor patient prognosis. The stomach pathogen, Helicobacter pylori ( H. pylori ), was recently proposed to stimulate c-Met phosphorylation dependent upon interaction of c-Met with the bacterial CagA protein required for H. pylori -induced cancer cell motility and invasion.

Materials and methods

In this report, we employed short hairpin RNA (shRNA), western blot analysis using antibodies recognizing phosphorylation at discrete c-Met residues, and immunofluorescence microscopy to investigate the CagA-c-Met interaction.

Results

The data showed that shRNA-mediated c-Met knockdown did not reduce H. pylori -induced cell motility, suggesting that c-Met wa

SUBMITTER: Snider JL 

PROVIDER: S-EPMC2687142 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature