PPAR- inhibitor T0070907 on cell growth inhibition of human nasopharyngeal carcinoma.docVIP

 PAGE \* MERGEFORMAT 19 PPAR- inhibitor T0070907 on cell growth inhibition of human nasopharyngeal carcinoma On: Sun Yueli Wu Mingwei Zengzhao Lei Sun Jiancai Yuchenxianli Jianzhaoqingyu [Abstract] [Objective] To investigate the PPAR- selective inhibitor T0070907 of nasopharyngeal carcinoma (NPC) cells in vitro and its mechanism. [Method] RT-PCR and Western blotting, PPAR- receptor in five NPC cell strains (CNE1, CNE2, HONE1, SUNE1 and 5-8F) in the expression of mRNA and protein levels; MTT assay T0070907 on cell growth of NPC; flow cytometry and Western blotting, T0070907 on cell cycle and the NPC cell cycle related protein expression. [results] PPAR- in five were expressed in NPC cells; T0070907 on the growth of NPC cell lines was inhibited in a concentration and time dependent; T0070907 role in NPC cells and CNE1 After CNE2, G2 / M phase cells increased gradually, and with the increase of concentration, the difference between the groups was statistically significant (P lt;0.05). In addition, with increasing concentrations of T0070907 treatment, NPC cells cell cycle-related proteins Cyclin A, Cyclin B1, Cdc2, Cdk2 protein gradually decreased, expression of inactive pCdc2 is gradually increased. [Conclusion] PPAR- inhibitor T0070907 can inhibit NPC cell protein expression of PPAR-, and through the cell cycle-related proteins Cyclin A, Cyclin B1, Cdc2, Cdk2, pCdc2 regulation of such proteins leads to cell cycle G2 / M phase arrest, thereby inhibiting the growth of NPC cells. [Keywords:] PPAR-; NPC; T0070907; cell cycle; G2 / M phase Abstract: [Objective] PPAR- (peroxisome proliferator-activated receptor-) antagonists have been documented to induce cancer cell proliferation inhibition and apoptosis. In the present study PPAR-’s effect on cell growth of NPC cell lines and the possible mechanism was investigated via its selective inhibitor T0070907. [Methods] PPAR- mRNA and protein expression in five human NPC cell lines (CNE1, CNE2, HONE1, SUNE1, and