[Effects of rosiglitazone on the Hep-2 cell proliferation, cell cycle and COX-2 expression].
OBJECTIVE
To explore the effect of rosiglitazone (ROS) on proliferation of human laryngeal carcinoma Hep-2 cells and it's mechanism.


METHODS
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.


RESULTS
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).


CONCLUSIONS
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.
Zhang
Yong
Y
Department Otorhinolaryngology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. yongzhangmail@126.com
Lou
Weihua
W
Zhang
Junhui
J
D017209:Apoptosis / Q000187:drug effects; D002294:Carcinoma, Squamous Cell / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007822:Laryngeal Neoplasms / Q000378:metabolism; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology*
D007004:Hypoglycemic Agents; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human