米非司酮诱导人宫颈癌Hela细胞凋亡机制的研究

Mechanism of cell apoptosis induced by mifepristone in human cervical carcinoma cell line Hela

目的探讨米非司酮(MIF)对人宫颈癌Hela细胞的凋亡诱导作用及作用机制。方法体外培养人宫颈癌Hela细胞,流式细胞技术分析不同浓度米非司酮对Hela细胞凋亡率及细胞周期分布的影响,用Western blot法检测米非司酮对Hela细胞中NF-κB p65蛋白表达水平的影响。结果 5、10、20μmol/L的米非司酮均能使Hela细胞凋亡率明显增加,使S期、G2/M期细胞比例减少,G0/G1期细胞比例显著增加,且作用呈剂量依赖性;随着米非司酮浓度的增加,Hela细胞中NF-κB p65蛋白表达水平逐渐下降。结论米非司酮可能通过NF-κB信号通路下调NF-κB p65蛋白表达,从而调节细胞周期,诱导Hela细胞凋亡。

Objective To investigate the regulatory effect of mifepristone on the cell apoptosis of human cervical cancer cell line Hela and the underlying mechanisms.Methods Human cervical cancer cell line Hela was cultured in vitro.Flow cytometry analysis technique was used to determine the changes of cell cycle distribution and cell apoptosis percentage after treatment with different concentrations of mifepristone.Western blot was performed to examine the effect of mifepristone on the expression of NF-κB p65 protein of Hela cell line.Results 5,10 and 20 μmol/L mifepristone significantly increased the cell apoptosis percentage and the proportion of cells in G0/G1 phase of Hela cells and decreased the proportion of cells in S and G2/M phases in a dose-depending manner.With the increase of mifepristone concentrations,the expression of NF-κB p65 was gradually downregulated in Hela cells.Conclusion Mifepristone can regulate cell cycle distribution and accelerate cell apoptosis by downregulating the expression of NF-κB p65 protein in cell line Hela via NF-κB signaling pathway.