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[Effects of rosiglitazone on the Hep-2 cell proliferation, cell cycle and COX-2 expression]
Yong Zhang1, Weihua Lou, Junhui Zhang
1Department Otorhinolaryngology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. yongzhangmail@126.com
Objective:
To explore the effect of rosiglitazone (ROS) on proliferation of human laryngeal carcinoma Hep-2 cells and it's mechanism.
Method:
Methabenzthiazuron (MTT) was used to observe the proliferation of human laryngeal carcinoma Hep-2 cells by various concentrations of ROS at different times. Flow cytometry (FCM) used to measure the cell cycle and apoptosis rate. RT-PCR was used to measure the expression of cyclooxygenase-2 (COX-2) mRNA.
Result:
The inhibited growth of ROS to Hep-2 cells in a dose-dependent and time-dependent manner (P < 0.01). The cell cycle was arrested in G0/G1 phase, which with a typical sub G1 peak, and the apoptosis rate increased in a time-dependent manner (P < 0.05). The expression of COX-2 mRNA in Hep-2 cells was significantly down-regulated by ROS (P < 0.01).
Conclusion:
The function of growth inhibition and apoptosis induction of ROS on human laryngeal cancer Hep-2 cells was obvious, and its mechanism was related to block cell cycle at the G0/G1 phase and decrease the expression of COX-2.
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