Journal
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Volume 67, Issue 6, Pages 461-465Publisher
ELSEVIER SCI LTD
DOI: 10.1054/plef.2002.0457
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Funding
- NHLBI NIH HHS [HL-46296] Funding Source: Medline
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15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD(+)-dependent oxidation of 15(S)-hydroxyl group of prostaglandins and has been considered a key enzyme involved in biological inactivation of prostaglandins. This enzyme is markedly induced by androgens in hormone-sensitive human prostate cancer cells (Tong M.,Tai H. H. Biochem Biophys Res Commun 2000; 276:77-81) and may be involved in tumorigenesis. Inhibition of this enzyme may be of value in anticancer therapy Non-steroidal anti-inflammatory drugs (NSAIDs) which inhibit cyclooxygenases (COXs) have been shown to be chemopreventive in epidemiological and animal-model studies. However, chemoprevention by these drugs may not be directly related to their inhibition of COXs. Other targets may be also involved in their chemopreventive activity. We have examined a variety of NSAIDs including COX-2 selective inhibitors, peroxisome proliferator-activated receptor (PPAR)gamma agonists and phytophenolic compounds which have been shown to be chemopreventive for their effect on 15-PGDH. It was found that most of these compounds were potent inhibitors of 15-PGDH. Among these compounds, ciglitazone appeared to be the most powerful inhibitor (IC(50)=2.7 muM). Inhibition by ciglitazone was non-competitive with respect to NAD(+) and uncompetitive with respect to PGE(2). (C) 2002 Elsevier Science Ltd. All rights reserved.
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