二羟异黄酮诱导乳腺癌MCF-7细胞凋亡的分子机制  

Molecular mechanism of daidzein-induced MCF-7 apoptosis in mammary cancer

作　　者：侯倩[1] 孙向楠 侯立朝[3] 雷初朝[4] 王枫[1] 

机构地区：[1]解放军第四军医大学军事预防医学系营养与食品卫生学教研室 [2]解放军71345部队医院门诊部 [3]解放军第四军医大学西京医院麻醉科 [4]西北农林科技大学动物科技学院

出　　处：《中国临床康复》2006年第11期117-119,共3页Chinese Journal of Clinical Rehabilitation

摘　　要：目的:分析植物雌激素二羟异黄酮诱导乳腺癌MCF-7细胞凋亡的分子机制和信号途径。方法:①实验于2005-11/2006-01在解放军第四军医大学军事预防医学系营养与食品卫生学教研室完成。②用十二孔培养板于细胞培养箱培养乳腺癌MCF-7细胞株(本实验室冻存)至对数生长期,施加终浓度分别为0,5,10,20,40μmol/L的二羟异黄酮(购自Sigma公司,4℃储存),作用24h后收集细胞,采用反转录聚合酶链反应方法检测cyclinE1,cdk2和p21表达水平。③计量资料差异比较采用单因素方差分析。结果:二羟异黄酮终浓度为0,10,20,40μmol/L时,细胞周期素cyclinE1和cdk2与β-actin基因条带的A值比值依次下降(P<0.05);p21与β-actin基因条带的A值比值依次上调(P<0.05);二羟异黄酮终浓度为0,5μmol/L时,cyclinE1,cdk2,p21与β-actin基因条带的A值比差异不明显(P>0.05)。结论:二羟异黄酮诱导乳腺癌MCF-7细胞凋亡可能是通过p21-cyclinE1/CDK2这条信号通路,且这种诱导呈剂量依赖性。AIM： To investigate the molecular mechanism and signal pathway of MCF- 7 apoptosis of patients with mammary cancer induced by daidzein. METHODS： The experiment was completed at the Department of Trophology ＆ Food Hygiene of Faculty of Military Preventive Medicine, the Fourth Military Medical University of Chinese PLA between November 2005 and January 2006. Twelve-well plate cultured breast cancer cell line MCF-7 cells were treated in exponential phase with daidzein at concentration of 0, 5, 10, 20 and 40 μmol/L （provided by Signm Company, 4 ℃）. Cells were harvested for detection of the expressions of cyclin El, cdk2 and p21 after 24-hour by reverse transcription-polymerase chain reaction （RT-PCR）. Measurement data were compared with one-way analysis of variance. RESULTS： When the concentrations of daidzein were 10, 20 and 40μmol/L, the expressions of cyclin E1 and cdk2 were down-regulated （P 〈 0.05）; while the expression of p21 up-regulated （P 〈 0.05）,but there was no remarkable change when the concentration of daidzein was 0 and 5μmol/L. CONCLUSION： The signal pathway of MCF-7 apeptosis induced by daidzein may be the p21-cyclin E1/CDK2 way, and it is dose-dependent.

关 键 词：乳腺肿瘤/药物疗法 细胞凋亡 肿瘤细胞 培养的 异黄酮类 

分 类 号：R730.1[医药卫生—肿瘤]