Activation of PPARγ inhibits cells growth of colorectal carcinoma via inducing cell apoptosis and cell cycle arrest

Objective:To investigate the expression of peroxisome proliferator-activated receptors (PPAR)γ and effect of PPARγ activation on cells growth in colorectal carcinoma (CRC) cell line HT-29. Methods:HT-29 were treated with rosiglitazone (PPARγ selective ligands) and 15d-PGJ-2. PPARγ mRNA and protein expression was detected by using reverse-transcriptase polymerase chain reaction and Western blotting. Cell proliferation was evaluated by MTT assay. Apoptosis was observed by fluorescence microscopy and TUNEL assay. The cell cycle was measured by flow cytometry using propidium iodide staining. Results:PPARγ mRNA and protein expression was detected in HT-29 cells. Cell proliferation was inhibited by rosiglitazone and 15d-PGJ-2 in a time-and concentration-dependent manner. HT-29 cells showed typical apoptosis changes after PPARγ activation. The apoptosis rate was (17.3±1.9)% and (20.8±2.9)% after treatment with 10 μmol/L rosiglitazone for 48 h and 15d-PGJ-2 for 24 h,respectively. The difference was significant compared with control (3.86%±0.49%,P0.05). Treatment with rosiglitazone and 15d-PGJ-2 arrested HT-29 cells at G_0/G_1 phase. The difference was significant compared with control (P0.05). Conclutions: PPARγ was expressed in HT-29 cells and activation of PPARγ inhibited CRC cell growth via inducing apoptosis and cell cycle arrest. PPARγ will be a novel target for treatment of CRC in humans.