The effect of the proteasome inhibitor combined with pshSTAT3 on proliferation and apoptosis in human laryngeal squamous cell carcinoma Hep-2 cell line
- VernacularTitle:蛋白酶体抑制剂联合pshSTAT3对喉癌细胞增殖及凋亡的影响
- Author:
Huiping ZHANG
;
Xiaoming LI
;
Xiuying LU
- Publication Type:Journal Article
- Keywords:
proteasome inhibitor;
laryngeal neoplasm;
STAT3;
RNA interference
- From:
China Oncology
2010;20(3):173-177
- CountryChina
- Language:Chinese
-
Abstract:
Background and purpose:Proteasome inhibitors constitute a novel class of antitumor agents that has a complex mechanism of action.Previous studies have confirmed that proteasome inhibitor MG-132 can significantly inhibit Hep-2 cell growth and induce cell apoptosis in a manner that is dependent on dosage and time.But it also induced p-STAT3 protein expression.The aim of this study was to explore whether the STAT3 gene can,by transfecting short hair pin RNA(shRNA),enhance the anti-tumor effect of MG-132 on human laryngeal carcinoma cells.Methods:Hep-2 cells were plated into 96-well and 6-well plates and incubated overnight.Then,they were treated with MG-132 alone and combined with pshSTAT3.Their cell growth was detected by MTT assay,and apoptosis was examined with flow cytometry.The protein expression of p-STAT3 was detected by Western blotting.Results:MTT assay showed that a combined group inhibited the proliferation of Hep-2 cells compared to the MG-132 group and pshSTAT3 group(P＜0.01).Flow cytometry showed that apoptosis of the combined group was significantly higher than the MG-132 group and pshSTAT3 group (P＜0.01).Western blotting showed that the p-STAT3 protein expression up-regulation was observed in the MG-132 group,whereas down-regulation was expressed in the combined group and pshSTAT3 group.Conclusion:The shRNA targeting STAT3 gene can prevent the up-regulation of p-STAT3 protein following a MG-132 treatment thereby significantly enhancing the anti-tunlor effect of the protease inhibitor,MG-132,on human laryngeal carcinoma cells.
