中文摘要：

目的：研究选择复制性腺病毒M4对卵巢癌细胞系OV2008的体外治疗作用并初步探讨其机制。方法：选择复制性腺病毒M4感染卵巢癌细胞系OV2008后,MTT法检测M4对OV2008细胞增殖抑制情况;流式细胞术检测M4对OV2008细胞凋亡的影响;PI法检测M4对OV2008细胞周期的影响,W estern blot法检测感染M4后STAT3蛋白以及其下游靶蛋白表达的改变。结果：选择复制性腺病毒M4能明显抑制OV2008细胞的增殖（P〈0.05）,并且能促进OV2008细胞的凋亡（P〈0.05）,PI法检测发现M4可以引起细胞G2-M期阻滞。W estern blot检测发现感染M4后STAT3蛋白及其靶蛋白survivin,Cyclin D1,Bcl-xl,p-STAT3的表达水平明显降低（P〈0.05）。结论：M4在体外对卵巢癌细胞系OV2008有非常好的治疗效果,其机制可能是因为M4能封闭卵巢癌细胞系中的STAT3基因,从而进一步促使p-STAT3蛋白以及其下游靶蛋白survivin,Bcl-xl,Cyclin D1等的表达降低,最终导致OV2008细胞的凋亡。

英文摘要：

Objective：To investigate the in vitro therapeutic effect of M4 on ovarian cancer cell line OV2008 and its rudiment mechanism.Methods：After the infection of M4 to OV2008,the proliferation inhibition rate of OV2008 was detected by MTT.The apoptotic rate was detected by flow cytometry;PI was used to detect the cycle change of OV2008.Western blot was used to detect the protein expression of STAT3 and its target protein.Results：After infection,the proliferation of OV2008 was inhibited（P0.05）,and the apoptotic rate of OV2008 was much higher than controls（P0.05）;the percentage of G2-M phase of OV2008 was increased after M4 infected.The protein expression levels of STAT3 and its target protein survivin,Bcl-xl,cyclin D1 were decreased（P0.05）.Conclusion：M4 had a potent therapeutic effect on ovarian cancer cell line OV2008 in vitro.Its rudiment mechanism may be that M4 blocked the expression of STAT3,and then decreased the expression of p-STAT3 and its target protein survivin,Bcl-xl,Cyclin D1,etc,eventually resulted in the apoptosis of OV2008 cells.