HSP90抑制剂对食管鳞癌细胞株TE-1凋亡的影响及作用机制

Effect of HSP90 inhibitor on apoptosis in esophageal squamous carcinoma cell TE-1 and its mechanism

目的探讨抑制热休克蛋白90(Hsp90)对食管鳞癌细胞株TE-1凋亡的影响。方法采用不同浓度(0.25、0.5、1.0、2.0μmol/L)、不同时间(24、48、72 h)HSP90抑制剂17-烯丙胺-17-脱甲氧格尔德霉素(17-AAG)处理食管鳞癌细胞株TE-1,分别采用MTT法、流式细胞仪及western blot检测细胞增殖、细胞凋亡及Hsp90、Hsp70、Akt、Fas蛋白表达。结果 17-AAG对TE-1细胞体外增殖抑制率和细胞凋亡率有明显促进作用,并呈现时间-剂量依赖性。17-AAG处理后TE-1细胞Hsp90、Akt蛋白表达明显降低,Hsp70、Fas蛋白表达明显上调。结论 17-AAG可显著抑制TE-1增殖,促进凋亡,其机制可能是通过抑制Hsp90活性、影响其相关信号通路所致。

Objective To evaluate the effect of inhibition Heat shock protein 90(HSP90) on apoptosis in esophageal squamous carcinoma cell TE-1.Methods TE-1 were treated with different time(24 h,48 h or 72 h)and different concentrations(0.25 μmol/L,0.5 μmol/L,1.0 μmol/L or 2.0 μmol/L)of 17-allylamio-17-desmethoxygeldanamycin(17-AAG).The cell proliferation,apoptosis and protein expression of Hsp90,Hsp70,Akt and Fas were determined by MTT method,flow cytometry and western blot.Results The 17-AAG on TE-1 cell in vitro proliferation inhibition and apoptosis rate had obvious promoting effect,and time-dose dependent.After curcumin treatment,the protein expression of Hsp90 and Akt significantly reduced,Hsp70 and Fas significantly increased.Conclusion 17-AAG can significantly inhibit the proliferation of TE-1,promote apoptosis,its mechanism may be through inhibiting Hsp90 activity and influence the related signaling pathway.