Effects of rosiglitazone on the Hep-2 cell proliferation, cell cycle and COX-2 expression.
- Author:
Yong ZHANG
1
;
Weihua LOU
;
Junhui ZHANG
Author Information
1. Department Otorhinolaryngology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. yongzhangmail@126.com
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Carcinoma, Squamous Cell;
metabolism;
Cell Cycle;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cyclooxygenase 2;
metabolism;
Humans;
Hypoglycemic Agents;
pharmacology;
Laryngeal Neoplasms;
metabolism;
Rosiglitazone;
Thiazolidinediones;
pharmacology
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2010;24(7):315-317
- CountryChina
- Language:Chinese
-
Abstract:
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.
