Peroxisome proliferator activator-receptor (PPAR)-γ ligand induces growth arrest of cancer cells through apoptosis. In this study, we examined the effects of PPAR-γ inhibitors on cell proliferation in renal cell carcinoma (RCC), bladder tumor (BT), and prostatic carcinoma (PC) cell lines. We investigated the inhibitory effect of PPAR-γ ligands, troglitazone and 15-deoxy-Δ12,14-prostaglandin J2 (15dPGJ2) on RCC, BT and PC-derived cell lines using MTT assay and Hoechst staining. PPAR-γ ligands (troglitazone and 15dPGJ2) induced the reduction of cell viability with the half-maximal concentration of growth inhibition of RCC, BT, and PC cell lines. Furthermore, counting cells at days 1, 2 and 3, clearly showed marked inhibition of cell proliferation using troglitazone and 15dPGJ2. All PPAR-γ inhibitors stopped the growth of all RCC, BT and PC cells. Cells treated with PPAR-γ inhibitors showed chromatin condensation, cellular shrinkage, small membrane-bound bodies (apoptotic bodies), and cytoplasmic condensation. These cellular changes were typically redundant characteristics of apoptosis. PPAR-γ ligands may mediate potent antiproliferative effects against RCC, BT and PC cells through differentiation. Thus, PPAR-γ may become a new target in treatment of urological tumors.

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