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Originally published In Press as doi:10.1074/jbc.M908890199 on March 10, 2000
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J Biol Chem, Vol. 275, Issue 20, 15090-15098, May 19, 2000

Bile Acid-induced Activation of Activator Protein-1 Requires Both Extracellular Signal-regulated Kinase and Protein Kinase C Signaling*

Dianhua Qiao, Weixing Chen, Elias D. Stratagoules, and Jesse D. MartinezDagger

From the Arizona Cancer Center, Department of Radiation Oncology, University of Arizona, Tucson, Arizona 85724

Elevated concentrations of fecal bile aids are known to promote colon cancer and increasing evidence suggests that alterations in cellular signaling and gene expression may play an important role in this process. In this study, we examined the molecular mechanisms underlying bile acid-mediated gene regulation using GADD153 as our model gene. Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor was crucial for deoxycholic acid (DCA)-mediated GADD153 gene transcription. Electrophoretic mobility shift assays and transient transfection analyses demonstrated that both DNA binding and transactivation activities of AP-1 were induced by DCA in a dose-dependent manner. The AP-1 complex induced by DCA consisted of JunD, Fra-1, and c-Fos. Examination of the signaling pathways stimulated by DCA showed that extracellular signal-regulated kinases (ERKs) were required for AP-1 activation. Inhibition of ERK by the mitogen-activated protein kinase/ERK kinase inhibitor PD 98059 or by expression of a dominant negative mutant ERK suppressed AP-1 activation. Notably, the PKC inhibitor, calphostin C, also abolished DCA-induced AP-1 activation but did not affect DCA-mediated ERK activation, suggesting that ERK and PKC function in separate signaling pathways that cooperatively mediate DCA-induced AP-1 activation. Hence, bile acid-stimulated signaling appears to converge on the AP-1 protooncogene.

* This work was supported by National Institutes of Health Grant CA-72008 and Cancer Center Core Grant CA-23074.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.

Dagger To whom correspondence should be addressed: Dept. of Radiation Oncology, P.O. Box 245024, 1501 N. Campbell Ave., Tucson, AZ 85724. Tel.: 520-626-4250; Fax: 520-626-4480; E-mail: jmartinez@azcc.arizona.edu.

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