米非司酮、维生素D3对乳腺癌细胞株MCF-7生长和凋亡的影响

目的:探讨米非司酮(RU486)和维生素D3(VitD3)对乳腺癌细胞株MCF-7生长和凋亡的影响,尤其是二者高浓度联合应用与单独高浓度应用之间的差异。方法:将MCF-7细胞株分别加入乙醇、VitD3和RU486。细胞培养24小时、48小时和72小时置光镜下观察细胞形态,利用体视学的方法进行计算细胞生存抑制率。72小时送流式细胞仪检查细胞分期、细胞凋亡率,经免疫组化、PI染色后行p53蛋白水平测定。结果:24小时、48小时、72小时低浓度组细胞生存抑制率与对照组乙醇相比较变化不大,而高浓度组和对照组相比较细胞生长抑制率明显升高。48小时比24小时抑制作用明显,72小时亦比48小时抑制作用明显。VitD310-7M RU48610-5M组比VitD310-7M组和RU48610-5M组72小时后的细胞生长抑制率明显升高。VitD310-7M组、RU48610-5M组、VitD310-7M RU48610-5M组较乙醇对照组相比,p53蛋白活化分子含量明显降低。结论:(1)RU486及VitD3的抗肿瘤作用有时间依赖性和剂量依赖性。(2)经析因分析后发现VitD310-7M和RU48610-5M两组具有交互作用(P<0.05),联合应用二者可以提高抗肿瘤作用。(3)RU486和VitD3可以引起乳腺癌细胞的凋亡,可能是通过一种或几种途径最终引起了p53蛋白的减少,推测其基因属突变型。

The effects of mifepristone,1,25-(OH)2-VitD3 on the growth and apoptosis of breast cancer cell line MCF-7

Objective:To study the effects of mifepristone(RU486)and 1,25-(OH)2-VitD3 on the growth and apoptosis of breast cancer cells clone MCF-7,especially to study the different effects between the combined high concentration and single high concentration,to find out if there is some interactions between them and to explore the possible mechanism.Methods:Treated the MCF-7cell line with alcohol,RU486 and VitD3,observed the cellular morph by lightmicroscopy after 24 hours,48 hours and 72 hours respectively,calculated the ratios of inhibition of cellular growth and took photos of them by means of somatoptogy cytometry then measure the level of p53 protein after immunohistochemistry and PI dying.Results:There wasn't significant difference of the inhibition rate of cellular growth between low concentration groups and the standard group treated with alcohol after 24 hours,48 hours and 72 hours,while the rate of the high concentration groups rised significantly.Furthermore,the ratio after 48 hours was much higher than that of 24 hours and so was the ratio of 72 hours than that of 48 hours.The mixed high concentration group was different from the the others.The factorial analysis suggested that there was interaction between the mixed high and the signal high concentration(P<0.05),while the level of p53 protein active molecular of the high concentration group were lower.Conclusion:The antitumor function of RU486 and VitD3 are time and dose-dependent.Factorial analysis suggests that there is a cooperative effection between VitD3 10-7M and RU486 10-5M.RU486 and VitD3 can induce the cells' apoptosis.The apoptosis causes the decrease of p53 protein in one or several ways.This bind of gene must be mutation-typed.