三苯氧胺治疗乳腺癌分子机制及其与CDK4、PCNA的关系  

STUDY ON RELATIONS ABOUT MA782 CELL APOPTOSIS INDUCED BY TAM WITH CDK4 AND PCNA

作　　者：吴建芳[1] 

机构地区：[1]青海大学医学院实验诊断教研室

出　　处：《青海医学院学报》2006年第4期234-237,共4页Journal of Qinghai Medical College

摘　　要：目的探讨三苯氧胺(TAM)治疗乳腺癌分子作用机制及其与细胞周期的关系。方法TAM作用于ER(-)小鼠乳腺癌MA782细胞,用流式细胞仪检测细胞凋亡率和细胞周期分布;MTT法检测细胞增殖活性;免疫法检测CDK4、PCNA蛋白表达量变化值,同时用病理图像分析软件进行半定量分析。结果TAM(6、10μmol/L)在体外能明显抑制MA782细胞生长,诱导细胞凋亡,TAM(6、10μmol/L)作用于细胞24 h后,细胞凋亡率分别为7.04%、19.04%,与对照组比较结果有明显差异,TAM(10μmol/L)作用于细胞24、48 h后细胞凋亡率从19.04%上升到51.27%,两时间段之间差异显著。免疫组织化学染色结果显示TAM(2μmol/L)作用于细胞不同时间后,CDK4、PCNA蛋白表达量无明显变化,而6、10μmol/L TAM作用于细胞不同时间后,CDK4、PCNA蛋白表达量有不同程度的下降,与对照组相比差异显著(P<0.05或P<0.01)。结论TAM诱导MA782细胞凋亡的分子作用机制,可能与TAM下调细胞周期正性调节因子CDK4、PCNA蛋白表达量有关。Objective To study whether tamoxifen(TAM) can induce growth arrest and apoptosis of ER-negative MA782 mouse breast cancer cell line and to explore the molecular mechanisms.Methods MA782 cells were Cultured in RPMI 1640 medium with TAM.The proliferative activity of cells was detected by MTT methods,and cells apoptosis by flowcytometrey methods.The expression of cdk4?PCNA proteins were detected by immunohistochemical methods,the semiquantity of protein expression was analyzed by pathological image analysis software.Results TAM can induce growth arrest and apoptosis of cells.FCM results showed that there was cell apoptosis with 6 or 10 μmol/L TAM for 24 hours but not with 2 μmol/L TAM.The percentage of apoptosis was 7.04% and 19.04% respectively,then it went up from 19.04% to 51.27 % after 48 hours with 10 μmol/L TAM.There was no change of above proteins with 2 μmol/L TAM,But after 48?72h treated with 6 μmol/L or 10 μmol/L TAM,the level of cdk4?PCNA protein decreased.The differences were significant(P<0.01).Conclusion Down-regulation of cdk4?PCNA proteins may be one of the mechanisms of TAM induced MA782 cell growth inhibition and apoptosis.

关 键 词：TAM MA782细胞 细胞凋亡 CDK4 PCNA 

分 类 号：R737.9[医药卫生—肿瘤] R979.1[医药卫生—临床医学]