摘要
目的:探讨乙酰辅酶A羧化酶抑制剂TOFA对卵巢癌COC1细胞增殖能力的抑制作用及其机制。方法:采用细胞增殖/毒性检测试剂(CCK-8)检测不同浓度TOFA作用24、48、72h对卵巢癌细胞增殖抑制作用,流式细胞仪检测COC1的细胞周期变化情况,免疫印迹技术(Western blot)检测COC1细胞磷酸化AKT、ERK蛋白表达的变化。结果:不同浓度(1、5、10、20、50μg/ml)TOFA分别作用24、48、72h后,对卵巢癌细胞的增殖抑制作用呈时间和剂量依赖。5、10、20、50μg/ml TOFA处理48h后实验组和对照组相比,阻滞于G0/G1期的细胞数明显增加(P<0.05)。10μg/ml TOFA作用后,可上调磷酸化AKT蛋白表达,60min后磷酸化ERK蛋白表达抑制率为47%(P>0.05)。结论:TOFA对卵巢癌细胞增殖抑制作用呈时间和剂量依赖性,诱导细胞G0/G1期阻滞,抑制磷酸化ERK表达,TOFA发挥作用的机制可能与MAPK/ERK信号转导通路相关。
Objective：To investigate the influence of TOFA,a Acetyl CoA Carboxylase inhibitor,on cell growth of human ovarian cancer cell line COC1,and explore the mechanism.Method： COC1 cells were added with TOFA（1,5,10,20,50μg/ml） for 24,48,72hours,then cell proliferation was assessed by CCK-8.Cell cycle was detected by flow cytometry（FCM）.The expression of p-AKT,p-ERK in COC1 cells were detected by Western blot.Results： The prolif-eration of COC1 cells was detected in dose-and time-dependent after treating with TOFA（P 0.05）.When added with 5,10,20,50μg/ml TOFA for 48 hours,COC1 cells were arrested in G0 /G1（P 0.05）.10μg/ml TOFA treatment increased the expression of p-AKT（P 0.05）.The expression of p-ERK was decreased after 60 minutes.Conclusion： TOFA inhibited the pro-liferation of COC1 in time-and dose-dependent,and arrested cells in G0 /G1.The mechanism of the effect can be correlated with MAPK/ERK signal transduction pathways.
出处
《现代妇产科进展》
CSCD
北大核心
2011年第8期597-599,共3页
Progress in Obstetrics and Gynecology
基金
上海市科委学科带头人基金项目(No:08XD14027)
上海交通大学医学院博士创新基金(No:BXJ201023)
上海教委重点学科
上海市妇科肿瘤重点实验室建设项目(No:09dz2200300)
