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Peroxisome Proliferator-Activated Receptor- Suppresses Cyclooxygenase-2 Expression in Human Prostate Cells

Department of Clinical Cancer Prevention, University of Texas M.D. Anderson Cancer Center, Houston, Texas

Requests for reprints: David G. Menter, Department of Clinical Cancer Prevention, Unit 236, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: 713-792-0626; Fax: 713-794-4403. E-mail: dmenter{at}mdanderson.org

Recent studies have found that cyclooxygenase-2 (COX-2) protein expression was low and inducible with cytokines in prostate cancer cells (in the absence of serum) and that, in contrast, COX-2 expression was high in normal prostate epithelial cells (EC). Peroxisome proliferator-activated receptor- (PPAR-) was expressed at high levels in the prostate cancer cell line PC-3 but not in ECs. In contrast to previous findings by others, PPAR- ligands did not induce PPAR- expression in EC or PC-3. The present study examined the relationship between PPAR- and COX-2 expression patterns in EC and PC-3 in the presence and absence of serum and/or the PPAR- agonist 15-deoxy-12,14-prostaglandin J₂ (15d-PGJ₂). We also evaluated the effects that the forced expression of PPAR-1 and PPAR-2 had on COX-2 in ECs. We found that expression of PPAR- and COX-2 protein was inversely correlated in ECs and PC-3. Low COX-2 expression in PC-3 was up-regulated by serum, and 15d-PGJ₂ blocked serum-induced COX-2 expression and activity in a dose-dependent manner. 15d-PGJ₂ had no effect on COX-2 expression in ECs or PPAR- expression in either cell type. However, forced expression of PPAR-1 or PPAR-2 in ECs suppressed the high level of endogenous COX-2. This effect was not isoform specific and was augmented by 15d-PGJ₂. The present study showed that PPAR- activation can be an important regulator of COX-2 in prostate cells and may be an important target for prostate cancer chemoprevention.

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