FoxO3a在三氧化二砷诱导的人乳腺癌MCF-7细胞凋亡中的表达和意义
Expression and Significance of FoxO3a in MCF-7 Cells Apoptosis Induced by Arsenic Trioxide
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摘要: 目的 探讨FoxO3a在三氧化二砷(As2O3)诱导人乳腺癌细胞MCF-7凋亡过程中的表达变化及其可能的机制。方法 将不同浓度的As2O3(2.0、4.0、8.0μmol/L)与MCF-7细胞共同培养24h后，采用流式细胞术检测MCF-7细胞凋亡；采用免疫细胞化学及Western blot技术检测FoxO3a和Caspase-3蛋白的表达,各实验均设相应的阴性对照组。结果 经不同浓度As2O3作用后，MCF-7细胞凋亡率逐渐增加，分别为(6.26±0.94)%、(9.30±1.63)%和(13.02±3.82)%，且呈剂量依赖关系(rs=0.949, P<0.01)；免疫细胞化学染色显示FoxO3a蛋白胞核表达增强，且Caspase-3蛋白表达增强（P<0.05)；Western blot条带显示FoxO3a蛋白表达水平逐渐升高，且激活型Caspase-3蛋白表达水平逐渐升高（P<0.05)。结论 As2O3可通过增强FoxO3a蛋白的活性，激活Caspase-3蛋白的表达而诱导MCF-7细胞凋亡。Abstract: Objective To investigate the apoptosis of MCF-7 cells induced by different concentrations of As2O3 and expressions of FoxO3a and Caspase-3 protein. Metheds The apoptosis of human breast carcinoma MCF-7 cells treated for 24 hours with 2.0，4.0，8.0 μmol/L As2O3 respectively was detected by flow cytometry. The activities of FoxO3a and Caspase-3 proteins were examined by immunocytochemistry and Western blot in untreated or treated by As2O3. Results The rate of the apoptosis in MCF-7 cells treated by 2.0，4.0，8.0 μmol/L of As2O3 were (6.26±0.94)%, (9.30±1.63)% and (13.02±3.82)%, respectively. There were obvious dose-effect correlations between As2O3 and apoptosis (rs=0.949, P<0.01). As2O3 promoted the expression of nucleus-FoxO3a and Caspase-3 protein. Conclusion The results suggested that As2O3 could induce apoptosis of MCF-7 cells via FoxO3a protein activation and Caspase-3 protein up-regulation.
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