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Cell Growth & Differentiation Vol. 13, 375-385, August 2002
© 2002 American Association for Cancer Research

c-Jun NH2-terminal Kinase Pathway in Growth-promoting Effect of the G Protein-coupled Receptor Cholecystokinin B Receptor

A Protein Kinase C/Src-dependent-Mechanism1

Stephanie Dehez, Christiane Bierkamp, Aline Kowalski-Chauvel, Laurence Daulhac, Chantal Escrieut, Christiane Susini, Lucien Pradayrol, Daniel Fourmy and Catherine Seva2

INSERM U.531, Groupe de Recherche de Biologie et Pathologie Digestives, Institut Louis Bugnard, Bat. L3, 31403 Toulouse, France

The proliferative effects of gastrin on normal and malignant gastrointestinal tissues have been shown to be mediated by a G protein-coupled receptor (GPCR), the cholecystokinin B receptor. The c-Jun NH2-terminal kinase (JNK) pathway has been implicated in the regulation of mitogenesis by growth factors or cytokines. However, the contribution of this signaling cascade to the proliferative effects of GPCR remains largely unknown. Here, we show that cholecystokinin B receptor occupancy by gastrin leads to the activation of the JNK pathway. The mechanism involves certain protein kinase C isoforms and Src family kinases other than p60Src. The complex p130Cas/CrkII, known to be involved in JNK activation, is also activated in response to gastrin by a protein kinase C- and Src-dependent mechanism. However, gastrin-induced CrkII and JNK pathways are independent. Using a dominant negative mutant of c-Jun, we blocked the ability of gastrin to induce DNA synthesis, demonstrating a major role of the JNK pathway in the growth-promoting effect of a GPCR agonist.




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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2002 by the American Association of Cancer Research.