| 方坤 刘金成 曲灵美 常乃丹 宋印利.毛蕊异黄酮抑制SIRT1 促乳腺癌细胞MCF-7 凋亡[J].现代生物医学进展英文版,2015,15(23):4431-4434. |
| 毛蕊异黄酮抑制SIRT1 促乳腺癌细胞MCF-7 凋亡 |
| Calycosin Promotes Apoptosis of Breast Cancer Cells MCF-7through Inhibiting SIRT1 |
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| DOI： |
| 中文关键词: 毛蕊异黄酮 凋亡 MCF-7 细胞 SIRT1 Cleaved caspase-3 |
| 英文关键词: Calycosin Apoptosis MCF-7 cells SIRT1 Cleaved caspase-3 |
| 基金项目:黑龙江省卫生厅科研课题基金（2011-233，2012-785） |
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| 中文摘要: |
| 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（10 uM，50 uM，100 uM）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，100 uM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，
300 uM）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。 |
| 英文摘要: |
| Objective:To explore the apoptotic mechanism of breast cancer cells MCF-7 caused by calycosin (CAL).Methods:MTT technology was used to detect effects of low, mediumand high (10 uM, 50 uM, 100 uM) concentrations of CAL on cell viability.
Tunel assay was applied to identify the effects of different dosages of CAL on apoptosis. Western blot technology was used to verify the
effects of CAL on apoptotic related proteins SIRT1, p53 and cleaved caspase-3. Real-time PCR was applied to investigate the expression
of caspase-3 mRNA level.Results:CAL could decrease cells viability. CAL of 100滋M concentration promoted tumor cell apoptosis,
decreased protein expression of SIRT1, increased level of p53 and cleaved caspase-3. SIRT1 inhibitor (Nicotinamide, NAM, 300 uM)
significantly repressed the protein level of SIRT1, increased protein level of p53 and cleaved caspase-3 compared with CAL treated
group; SRT1720 (SIRT1 specific agonist) reversed the inhibitory effects of CAL on protein level of SIRT1, whereas the protein level of
p53 and cleaved caspase-3 were dominantly decreased.Conclusion:CAL can promote MCF-7 cells apoptosis, at least partly due to
downregulated protein level of SIRT1, thereby increasing important apoptotic related gene p53 and caspase-3. |
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