COX-2 inhibition, apoptosis, and chemoprevention by nonsteroidal anti-inflammatory drugs.
Non-steroidal anti-inflammatory drugs (NSAIDs) have as their common mechanism the inhibition of cyclooxygenase (COX) enzymes, of which two isoforms (COX-1 and COX-2) exist. The effect of NSAIDs on chemoprevention and tumor regression has been shown in animal models, epidemiologic studies, and in treatment of patients. The exact biochemical and cellular mechanisms underlying each of these phenomena is only partially understood. Processes that have been recently implicated as being important include the inhibition of tumor cell growth, prevention of angiogenesis, and induction of apoptosis in neoplastic cells.
Moore
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BC
Department of Chemistry and Biochemistry, Brigham Young University, Provo, Utah 84602, USA.
Simmons
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DL
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D017209:Apoptosis; D018360:Crystallography, X-Ray; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D004195:Disease Models, Animal; D006801:Humans; D007527:Isoenzymes / Q000037:antagonists & inhibitors*; D008565:Membrane Proteins; D051379:Mice; D015394:Molecular Structure; D009369:Neoplasms / Q000201:enzymology / Q000517:prevention & control*; D009389:Neovascularization, Pathologic / Q000201:enzymology / Q000517:prevention & control*; D011451:Prostaglandin-Endoperoxide Synthases
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases