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目的:探讨米非司酮对人子宫内膜癌细胞HEC-1-B体外增殖的影响及可能的作用机制。方法:体外培养人子宫内膜癌细胞HEC-1-B,不同浓度米非司酮处理细胞24～96 h后,用四甲基偶氮唑蓝比色法测定细胞增殖活性,流式细胞仪检测细胞周期,免疫组化方法检测凋亡相关蛋白Bcl-2和增殖相关抗原Ki-67蛋白的表达。结果:2.5 mg/L米非司酮作用72～96 h,5～20 mg/L米非司酮作用24～96 h,对人子宫内膜癌细胞HEC-1-B的生长有抑制作用(P<0.05),且呈明显的时间、浓度依赖性。5～20 mg/L米非司酮作用于HEC-1-B细胞24 h后,G0/G1期细胞概率上升,S期细胞概率下降(P<0.05),并呈明显的浓度依赖性,Bcl-2及Ki-67蛋白的表达水平亦下降(P<0.05),但无明显的浓度依赖性。结论:米非司酮能抑制人子宫内膜癌细胞HEC-1-B的生长,其机制可能与阻止细胞周期和促进细胞凋亡有关。
Objective: To investigate the effect of mifepristone on the proliferation of human endometrial carcinoma cell line HEC-1-B and its possible mechanism. Methods: Human endometrial carcinoma cell line HEC-1-B was cultured in vitro. The cells were treated with different concentrations of mifepristone for 24-96 h. The cell proliferation activity was measured by MTT method. The cell cycle was detected and the expression of Bcl-2 and Ki-67 protein were detected by immunohistochemistry. Results: Mifepristone 2.5 mg / L for 72-96 h and Mifepristone 5-20 mg / L for 24-96 h inhibited the growth of human endometrial carcinoma cell line HEC-1-B ( P <0.05), and showed significant time and concentration-dependent. After treated with 5-20 mg / L mifepristone for 24 h, the cell probability of G0 / G1 phase increased and the cell probability of S phase decreased (P <0.05), and the concentration of Bcl -2 and Ki-67 protein expression decreased (P <0.05), but no significant concentration-dependent. Conclusion: Mifepristone can inhibit the growth of human endometrial carcinoma cell line HEC-1-B, which may be related to the prevention of cell cycle and the promotion of apoptosis.