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Originally published In Press as doi:10.1074/jbc.M000959200 on March 19, 2000

J. Biol. Chem., Vol. 275, Issue 21, 16064-16072, May 26, 2000
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Helicobacter pylori Activates Mitogen-activated Protein Kinase Cascades and Induces Expression of the Proto-oncogenes c-fos and c-jun*

Tobias Meyer-ter-VehnDagger , Antonello Covacci§, Manfred Kist, and Heike L. PahlDagger ||

From the Dagger  Division of Experimental Anaesthesiology, University Hospital Freiburg, Center for Tumor Biology, P. O. Box 1120, 79106 Freiburg, Germany, the § IRIS-BIOCINE, Via Fiorentina 1, 53100 Siena, Italy, and the  Institut für Medizinische Mikrobiologie und Hygiene der Universität Freiburg, Hermann-Herder-Strasse 11, 79104 Freiburg, Germany

Helicobacter pylori is an etiological agent in the development of mucosa-associated lymphoid tissue lymphoma and gastric adenocarcinoma. Patients infected with H. pylori carry a 3-6-fold increased risk of developing cancer compared with uninfected individuals. H. pylori strains expressing the cytotoxin-associated antigen A (CagA) are more frequently associated with the development of neoplasia than cagA-negative strains. However, the molecular mechanism by which H. pylori causes neoplastic transformation remains unclear. Here we report that exposure of gastric epithelial cells to H. pylori induces activation of the transcription factor activator protein 1. Activation of the proto-oncogenes c-fos and c-jun is strongly induced. We show that H. pylori activates the ERK/MAP kinase cascade, resulting in Elk-1 phosphorylation and increased c-fos transcription. H. pylori strains that do not express CagA or that are mutated in cag genes encoded by the CagI pathogenicity island do not induce activator protein 1, MAP kinase activity, or c-fos or c-jun activation. Proto-oncogene activation may represent a crucial step in the pathomechanism of H. pylori induced neoplasia.

* This work was supported by Grant Pa 611/4-1 from the Deutsche Forschungsgemeinschaft and by the Alfried Krupp-Förderpreis (to H. L. P.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed. Tel.: 49-761-206-1530; Fax.: 49-761-206-1529; E-mail: pahl@uni-freiburg.de.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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