蛋白酶体抑制剂联合pshSTAT3对喉癌细胞增殖及凋亡的影响

背景与目的:蛋白酶体抑制剂是一种新型抗肿瘤靶向治疗药物,其作用机制复杂.本研究前期的工作已经证实,蛋白酶体抑制剂可以有效抑制人喉鳞癌Hep-2细胞的增殖并诱导其凋亡,但它同时也诱导了p-STAT3蛋白表达水平的升高.本研究旨在探讨pshSTAT3抑制p-STAT3蛋白表达能否增强蛋白酶体抑制剂MG-132对喉癌细胞的抗肿瘤作用.方法:以Hep-2细胞为实验对象,利用四甲基偶氮唑蓝(MTT)法、流式细胞术(flow cytometry,FCM)检测MG-132单独及联合pshSTAT3时,细胞增殖抑制率及凋亡率的变化;Western印迹法检测各组p-STAT3蛋白表达情况.结果:MTT榆测结果显示,联合组细胞的增殖抑制作用最强,与MG-132组及pshSTAT3组相比较差异均有统计学意义(P＜0.01).FCM检测结果显示,联合组细胞出现明显的凋亡峰,其凋亡率显著高于MG-132组和pshSTAT3组,差异极有统计学意义(P＜0.01).Western印迹法检测结果显示,经2.5μmol/L MG-132处理Hep-2细胞后P-STAT3蛋白表达显著增强;联合组及pshSTAT3组P-STAT3蛋白表达明显减弱.结论:pshSTAT3可以抑制MG-132诱导的p-STAT3蛋白表达,从而提高蛋白酶体抑制剂MG-132对喉癌细胞的抗肿瘤作用.

The effect of the proteasome inhibitor combined with pshSTAT3 on proliferation and apoptosis in human laryngeal squamous cell carcinoma Hep-2 cell line

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 hu...