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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。
Objective: To study the in vitro therapeutic effect of replicative adenovirus M4 on ovarian cancer cell line OV2008 and to explore its mechanism. Methods: The ovarian cancer cell line OV2008 was transfected with the replication-competent adenovirus M4. The proliferation of OV2008 cells was detected by MTT assay. The apoptosis of OV2008 cells was detected by flow cytometry. The PI assay was used to detect the effect of M4 on the cell cycle of OV2008 cells Western blot was used to detect the expression of STAT3 protein and its downstream target protein after M4 infection. Results: The replication-competent adenovirus M4 could significantly inhibit the proliferation of OV2008 cells (P <0.05) and promote the apoptosis of OV2008 cells (P <0.05). PI assay showed that M4 could induce cell G2-M arrest. Western blot showed that the expression of STAT3 and its target proteins survivin, Cyclin D1, Bcl-xl and p-STAT3 were significantly decreased after M4 infection (P <0.05). CONCLUSION: M4 has a very good therapeutic effect on ovarian cancer cell line OV2008 in vitro. The possible mechanism is that M4 can block the STAT3 gene in ovarian cancer cell lines and further promote the expression of p-STAT3 protein and its downstream target proteins survivin, Bcl -xl, Cyclin D1 and so reduce the expression, eventually leading to apoptosis of OV2008 cells.