Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARγ) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (PGZ)...Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARγ) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (PGZ) on proliferation of MGC803 cells was analyzed by MTT assay. Cell cycle was detected by flow cytometry (FCM). The expressions of PPARγ, cyclin D1 and cell cycle protein-dependent kinase CDK4 in MGC803 cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Treatment with 0.1-10 μmol/L PGZ for 96 h significantly inhibited cell proliferation. The proportion of MGC803 cells at G1 phase was significantly increased when treated with 10 μmol/L PGZ for 48, 72 and 96 h, and showed an apparent G1 phase arrest. The expression of PPARγ was at a low level in MGC803 cells and significantly up-regulated when treated with 10 μmol/L PGZ for 48 h (P < 0.01). The expression of CDK4 in MGC803 cells was remarkably down-regulated when treated with 10 μmol/L PGZ for 48 h and the expression of cyclin D1 was slightly down-regulated (P < 0.01). Conclusion: Activation of PPARγ significantly induced G1 phase arrest, which was associated with down-regulation of the expressions of CDK4 and cyclin D1.展开更多
基金This work was supported by grants from the National Natural Science Foundation of China （No. 30225037, 30400538, 30471991,30570731）；the 973 Program of China （No. 2006CB503909, 2004CB518603）；the ＂111＂ Project, and the Natural Science Foundation of Jiangsu Province （No. BK2004082, BK2006714）.
文摘Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARγ) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (PGZ) on proliferation of MGC803 cells was analyzed by MTT assay. Cell cycle was detected by flow cytometry (FCM). The expressions of PPARγ, cyclin D1 and cell cycle protein-dependent kinase CDK4 in MGC803 cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Treatment with 0.1-10 μmol/L PGZ for 96 h significantly inhibited cell proliferation. The proportion of MGC803 cells at G1 phase was significantly increased when treated with 10 μmol/L PGZ for 48, 72 and 96 h, and showed an apparent G1 phase arrest. The expression of PPARγ was at a low level in MGC803 cells and significantly up-regulated when treated with 10 μmol/L PGZ for 48 h (P < 0.01). The expression of CDK4 in MGC803 cells was remarkably down-regulated when treated with 10 μmol/L PGZ for 48 h and the expression of cyclin D1 was slightly down-regulated (P < 0.01). Conclusion: Activation of PPARγ significantly induced G1 phase arrest, which was associated with down-regulation of the expressions of CDK4 and cyclin D1.
