PMID:17164142

Citation	Eisinger, AL, Prescott, SM, Jones, DA and Stafforini, DM (2007) The role of cyclooxygenase-2 and prostaglandins in colon cancer. Prostaglandins Other Lipid Mediat. 82:147-54
Abstract	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.
Links	PubMed Online version:10.1016/j.prostaglandins.2006.05.026
Keywords	Adenomatous Polyposis Coli Protein/physiology; Animals; Colonic Neoplasms/physiopathology; Cyclooxygenase 2/physiology; Dinoprostone/physiology; Gene Expression Regulation, Neoplastic; Genes, APC/physiology; Humans; Prostaglandins/physiology; Signal Transduction/physiology; Up-Regulation; Wnt Proteins/physiology; beta Catenin/physiology
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Significance

Cyclooxygenase-2, COX-2, is overexpressed in colon cancer, suggesting a relationship between the pathway and signaling of COX-2 and colorectal carcinogens. When COX-2 activity is inhibited by sulindac, a metabolite of sulindac sulfoxide, the average diameter and number of polyps decreased in patients affected by colorectal cancers.

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
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References

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