The role of cyclooxygenase-2 and prostaglandins in colon cancer.
The temporal association between loss of function of the tumor suppressor adenomatous polyposis coli (APC) and overexpression of cyclooxygenase 2 (COX-2) has been demonstrated in vivo and has led to the hypothesis that APC regulates COX-2 expression. This could potentially occur through a variety of mechanisms including the well-characterized ability of APC to negatively regulate Wnt signaling and decrease expression of target genes. However, recent findings suggest that the products of COX-2 elicit effects that occur upstream of the beta-catenin/TCF/LEF pathway. This review will focus on the regulation of COX-2 by APC and the interplay between COX-2 and the Wnt signaling pathway.
Eisinger
Annie L
AL
Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, United States. annie.eisinger@hci.utah.edu
Prescott
Stephen M
SM
Jones
David A
DA
Stafforini
Diana M
DM
D025601:Adenomatous Polyposis Coli Protein / Q000502:physiology; D000818:Animals; D003110:Colonic Neoplasms / Q000503:physiopathology*; D051546:Cyclooxygenase 2 / Q000502:physiology*; D015232:Dinoprostone / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic; D017491:Genes, APC / Q000502:physiology; D006801:Humans; D011453:Prostaglandins / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D015854:Up-Regulation; D051153:Wnt Proteins / Q000502:physiology; D051176:beta Catenin / Q000502:physiology
D025601:Adenomatous Polyposis Coli Protein; D011453:Prostaglandins; D051153:Wnt Proteins; D051176:beta Catenin; D051546:Cyclooxygenase 2; D015232:Dinoprostone