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© The Rockefeller University Press, 0021-9525/2003/4/219 $5.00
The Journal of Cell Biology, Volume 161, Number 2, 219-219

H. pylori mobilizes cells

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 PLC, a mediator of cell polarity necessary for motility. CagA–PLC interactions mobilized infected cells through an ERK-dependent MAP kinase pathway, as inhibitors of MAP kinases or PLC blocked motility.

Unlike the gastric tumor cell line, a polarized canine kidney cell line does scatter in response to HGF. H pylori also induced c-Met–mediated motility in these cells, but did so through a PI3K-dependent pathway rather than through PLC, indicating that the bug uses alternative routes to motility depending on the cell type. The authors hope to look at animal models next to determine whether inappropriate activation of c-Met and the resulting mobilization of gastric cells is responsible for increased incidences of metastatic cancers in H. pylori infections.

Nicole LeBrasseur

lebrasn{at}rockefeller.edu

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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response

Yuri Churin, Laila Al-Ghoul, Oliver Kepp, Thomas F. Meyer, Walter Birchmeier, and Michael Naumann
J. Cell Biol. 2003 161: 249-255. [Abstract] [Full Text] [PDF]

This Article Full Text (PDF, 705K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by LeBrasseur, N. Search for Related Content PubMed Articles by LeBrasseur, N. Related Collections Related Article Social Bookmarking                            What's this?