NSAIDs (non-steroidal anti-inflammatory drugs) prevent colon and other cancers. The fact that NSAIDs inhibit the eicosanoid pathway prompted mechanistic drug-developmental work focusing on COX (cyclo-oxygenase) and its products. The increased prostaglandin E2 levels and the overexpression of COX-2 in colon and many other cancers provided the rationale for clinical trials with COX-2 inhibitors for cancer prevention or treatment. However, one COX-2 inhibitor has been withdrawn from the market because of cardiovascular side effects, and there are concerns about a class effect. Evidence suggests that COX-2 may not be the only, or the ideal, target for cancer prevention; for example, COX-2 is not expressed in human aberrant crypt foci, the earliest recognizable pre-malignant lesion in the colon; COX-2 is expressed in less than half of the adenomas; in vitro data show that NSAIDs do not require the presence of COX-2 to prevent cancer; in familial adenomatous polyposis, the COX-2 inhibitor, celecoxib, had a modest effect, which was weaker than that of a traditional NSAID; and COX-2-specific inhibitors have several COX-2-independent activities, which may account for part of their cancer-preventive properties. The multiple COX-2-indpendent targets, and the limitations of COX-2 inhibitors, suggest the need to explore targets other than COX-2.
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August 2005
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Conference Article|
August 01 2005
Is COX-2 a ‘collateral’ target in cancer prevention?
K. Kashfi;
K. Kashfi
*Department of Physiology and Pharmacology, City University of New York Medical School, NY 10031, U.S.A.
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B. Rigas
B. Rigas
1
†Division of Cancer Prevention, Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794-5200, U.S.A.
1To whom correspondence should be addressed (email basil.rigas@sunysb.edu).
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Publisher: Portland Press Ltd
Received:
March 22 2005
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2005 The Biochemical Society
2005
Biochem Soc Trans (2005) 33 (4): 724–727.
Article history
Received:
March 22 2005
Citation
K. Kashfi, B. Rigas; Is COX-2 a ‘collateral’ target in cancer prevention?. Biochem Soc Trans 1 August 2005; 33 (4): 724–727. doi: https://doi.org/10.1042/BST0330724
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