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Papers In Press, published online ahead of print April 5, 2001
J. Biol. Chem, 10.1074/jbc.M101801200
Submitted on February 27, 2001
Revised on March 23, 2001
Accepted on April 5, 2001

AP-1 transcription factor mediates bombesin-stimulated cyclooxygenase-2 expression in intestinal epithelial cells

Yan-Shi Guo, Mark R. Hellmich, Xiao Dong Wen, and Courtney M. Townsend Jr

Department of Surgery, The University of Texas Medical Branch, Galveston, TX 77555

Corresponding Author: ctownsen{at}utmb.edu

Colorectal carcinogenesis is a complex, multi-step process involving genetic alternations and progressive changes in signaling pathways regulating intestinal epithelial cell proliferation, differentiation and apoptosis. Although cyclooxgenase-2 (COX-2), gastrin-releasing peptide (GRP) and its receptor, GRP-R, are not normally expressed by the epithelial cells lining the human colon, the levels of all three proteins are aberrantly overexpressed in premalignant adenomatous polyps and colorectal carcinomas of humans. Overexpression of these proteins is associated with altered epithelial cell growth, adhesion and tumor cell invasiveness, both in vitro and in vivo; however, a mechanistic link between GRP-R-mediated signaling pathways and increased COX-2 overexpression has not been established. We report that bombesin (BBS), a homolog of GRP, potently stimulates the expression of COX-2 mRNA and protein as well as the release of PGE2 from a rat intestinal epithelial cell line engineered to express GRP-R. BBS stimulation of COX-2 expression requires an increase in [Ca2+]i, activation of extracellular signal-regulated kinase (ERK)-1 and -2 as well as p38MAPK and increased activation and expression of the transcription factors, Elk-1, ATF-2, c-Fos and c-Jun. These data suggest that the expression of GRP-R in intestinal epithelial cells may play a role in carcinogenesis by stimulating COX-2 overexpression through an AP-1-dependent pathway.


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