毛蕊异黄酮抑制SIRT1促乳腺癌细胞MCF-7凋亡

被引：7

作者：

方坤

刘金成

曲灵美

常乃丹

宋印利

机构：

[1] 哈尔滨医科大学大庆校区

来源：

现代生物医学进展 | 2015年 / 15卷 / 23期

关键词：

毛蕊异黄酮; 凋亡; MCF-7细胞; SIRT1; Cleaved caspase-3;

D O I：

10.13241/j.cnki.pmb.2015.23.008

中图分类号：

R737.9 [乳腺肿瘤];

学科分类号：

100214 [肿瘤学];

摘要：

目的:探讨毛蕊异黄酮促乳腺癌细胞MCF-7凋亡的机制。方法:MTT检测低、中、高(10μM,50μM,100μM)剂量的毛蕊异黄酮对细胞活力的影响;Tunel检测毛蕊异黄酮对细胞凋亡的影响;Western blot检测SIRT1,p53和cleaved caspase-3的蛋白表达;Real-time PCR检测caspase-3 mRNA的表达。结果:毛蕊异黄酮能够剂量依赖性地降低细胞活力,100μM剂量组的毛蕊异黄酮显著地促进肿瘤细胞凋亡并降低SIRT1,增加p53和cleaved caspase-3的蛋白表达。SIRT1抑制剂烟酰胺(Nicotinamide,NAM,300μM)组与毛蕊异黄酮处理组相比显著地抑制SIRT1的蛋白表达,p53和cleaved caspase-3蛋白表达水平进一步增加;SRT1720(SIRT1特异性激动剂)与毛蕊异黄酮共孵育组逆转SIRT1蛋白表达,降低p53和cleaved caspase-3的蛋白水平。结论:毛蕊异黄酮促进肿瘤细胞MCF-7的凋亡,部分可能是通过降低SIRT1的表达水平,从而增加p53和cleaved caspase-3的蛋白表达促进细胞凋亡。

引用

页码：4431 / 4434+4511 +4511

页数：5

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