三氧化二砷诱导卵巢癌细胞系SKOV3细胞凋亡的作用和机制

目的观察三氧化二砷(ATO)诱导人卵巢癌细胞系SKOV3细胞的凋亡作用和凋亡通路分子caspase 3、PARP,凋亡相关蛋白p-AKT、AKT蛋白表达的变化。方法分别用不同剂量的三氧化二砷作用人卵巢癌细胞系SKOV3细胞,应用MTT比色法检测培养48 h的细胞存活率,应用流式细胞仪测定培养48 h细胞凋亡的变化,免疫印迹法检测凋亡蛋白caspase 3、PARP和凋亡相关蛋白p-AKT、AKT的表达情况。结果 MTT示三氧化二砷能明显抑制SKOV3细胞增殖;流式细胞术显示三氧化二砷诱导SKOV3细胞凋亡,且具有明显的剂量依赖性;Western blotting检测发现药物能显著下调caspase 3、PARP、p-AKT的表达水平。结论三氧化二砷能显著抑制人卵巢癌细胞系SKOV3细胞增殖,诱导其凋亡,激活凋亡通路分子caspase 3、PARP,下调p-AKT蛋白表达水平,这可能是三氧化二砷诱导人卵巢癌细胞SKOV3细胞凋亡的作用机制。

Arsenic trioxide induced ovarian cancer cell line SKOV3 function and mechanism of apoptosis

Objective To observe the effect of Arsenic trioxide induced apoptosis and the change of protein expression of caspase 3, PARP, p - AKT and AKT in human ovarian cancer cell lines SKOV3. Methods The ovarian cancer cell lines SKOV3 was treated with Arsenic trioxide at various concentrations for 48 h. The inhibition of proliferation was measured by MTY. The apoptotic rates was detected by flow cytometry. The protein expression of caspase 3, PARP and p - AKT was detected by Western blotting. Results Arsenic trioxide inhibited the proliferation of SKOV3 cell significantly by MTT. Flow cytometry showed that Arsenic trioxide induced apoptosis and had an obvious dose - dependent in SKOV3 cell. Western boltting showed the protein expression of caspase 3, PARP and p - AKT were lower after drug intervention. Conclusion Arsenic trioxide can inhibit the proliferation and induce apoptosis of the ovarian cancer cell lines SKOV3 and inhibit the expressions of apoptotic pathway molecules caspase 3, PARP and apoptosis - related protein p - AKT, which may be the mechnism of action of arsenic trioxide induced apoptosis in ovarian cancer.