Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 462, Issue 1, Pages 1-12Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2007.03.013
Keywords
prostate cancer; PPAR gamma; c-myc; beta-catenin; cadherins; proliferation; GW9662; differentiation
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Peroxisome proliferator-activated receptor gamma (PPAR gamma) ligands seem to induce anticancer effects on prostate cancer cells, but the mechanism is not clear. The effect of PPAR gamma ligands omega-6 fatty acids and ciglitazone (2-15 mu M)-on proliferation, and apoptosis of LNCaP, PC-3, DU145, CA-K and BPH-K cells was studied. PPAR gamma ligands led to: (1) reduction of proliferation (20-50%) of all the studied cell lines, (2) stimulation of differentiation of prostate cancer cells through an increased expression (1.5-3-fold: LNCaP, DU145, BPH-K) or reexpression (PC-3, CA-K) of E-cadherin with parallel inhibition of N-cadherin expression (PC-3, CA-K) and (3) down-regulation (1-2-fold) of beta-catenin and c-myc expression. The selective PPAR gamma antagonist GW9662 abolished the effect of those ligands on prostate cancer cells. These results suggest that inhibition of beta-catenin and in effect c-myc expression through activation of PPAR gamma may help prostate cancer cells to restore several characteristics of normal prostate cells phenotype. (C) 2007 Elsevier Inc. All rights reserved.
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