H. pylori infection mobilizes gastric epithelial cells (right) by activating c-Met.

Helicobacter pylori infects the gastric track of more than half of the human population and is associated with an increased occurrence of invasive gastric cancers. On page 249, Churin et al. explain how this widespread bug turns tumors metastatic by corrupting a growth factor receptor.

H. pylori mobilizes infected epithelial cells on its course to pathogenicity. The authors now show that mobilization results from activation of the hepatocyte growth factor (HGF) receptor c-Met. During development and differentiation, HGF-induced activation of c-Met initiates cell migration events. Inhibition of c-Met expression by siRNA blocks H. pylori–induced motility. H. pylori corrupts c-Met signaling, however, by injecting host cells with the protein CagA. Binding of CagA to c-Met resulted in modulation of receptor activity and recruitment of PLCγ, a mediator of cell polarity necessary for...

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