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Sci. STKE, 29 March 2005
Vol. 2005, Issue 277, p. pe14
[DOI: 10.1126/stke.2772005pe14]

PERSPECTIVES

Orchestration of Aberrant Epithelial Signaling by Helicobacter pylori CagA

Richard M. Peek Jr.1*

1Division of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232-2279, USA; Department of Veterans Affairs Medical Center, Nashville, TN 37212-2637, USA.

Abstract: Persistent colonization by Helicobacter pylori is the strongest risk factor for distal gastric adenocarcinoma, and H. pylori strains that harbor the cag pathogenicity island further augment cancer risk. The H. pylori cag island encodes a secretion system, and the product of the terminal gene in the island (CagA) is translocated into host epithelial cells after bacterial attachment, where it undergoes tyrosine phosphorylation by Src kinases and binds the eukaryotic phosphatase SHP-2. Higashi et al. now demonstrate that CagA-dependent SHP-2 activation leads to sustained activation of ERK (extracellular signal-regulated kinase), culminating in morphological changes that mimic unrestrained stimulation by growth factors. These data implicate the cag island as a key mediator of pathogenic epithelial responses that may heighten the risk for gastric cancer.

*Contact information. Telephone: (615) 322-5200; Fax: (615) 343-6229; e-mail: richard.peek{at}vanderbilt.edu

Citation: R. M. Peek, Jr., Orchestration of Aberrant Epithelial Signaling by Helicobacter pylori CagA. Sci. STKE 2005, pe14 (2005).

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