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中国癌症防治杂志

中国癌症防治杂志 ›› 2013, Vol. 5 ›› Issue (2): 126-129.doi: 10.3969/j.issn.1674-5671.2013.02.10

• 临床研究 • 上一篇    下一篇

二甲双胍抑制乳腺癌MCF-7细胞作用的研究

  

  1. 山西医科大学研究生学院；山西医科大学第二医院乳腺外科
  • 出版日期:2013-06-25 发布日期:2013-06-27
  • 通讯作者: 王伏生 E-mail:wfs636491@163.com

Inhibitory effects of metformin on breast cancer cell line MCF-7

  • Online:2013-06-25 Published:2013-06-27

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8

摘要： 目的 初步探讨二甲双胍对乳腺癌MCF-7细胞的抑制作用。方法 将乳腺癌MCF-7细胞分为实验组和对照组，实验组用终浓度为16.56 g/L的二甲双胍培养，对照组不用二甲双胍干预。两组MCF-7细胞在相同条件下培养48 h后分别提取细胞总蛋白，应用Western blot法检测乳腺癌MCF-7细胞中NF-κB p65、Lin28B的表达情况。以RT-PCR法检测MCF-7细胞中microRNA let-7下游基因HMGA2、H-Ras的转录水平。结果 药物干预48 h后，乳腺癌MCF-7细胞中NF-κB p65、Lin28B的表达水平下降，差异有统计学意义（P＜0.05）。实验组乳腺癌MCF-7细胞中自我复制和多向分化的相关基因HMGA2、H-Ras的转录水平明显下降，2-△△Ct测得两种基因的表达分别下降85%和96%（P均＜0.05）。结论 16.56 g/L的二甲双胍能够有效地降低乳腺癌MCF-7细胞中NF-κB p65、Lin28B的表达，进一步抑制乳腺癌MCF-7细胞多向分化和自我复制相关基因HMGA2和H-Ras的表达，从而为二甲双胍抑制乳腺癌的复发和转移提供实验依据。

关键词:  , 乳腺肿瘤, 二甲双胍, NF-&kappa, B p65, Lin28B, HMGA2, H-Ras

Abstract: Objective To explore the mechanism of metformin in inhibiting breast cancer cell line MCF-7. Methods MCF-7 cells were cultured for 48 h in the presence or absence of 16.56 g/L metformin，total protein was extracted from cells and expression of nu-clear factor-kappa B（NF-κB） p65 and Lin28B were detected by Western blot. Furthermore， transcription levels of HMGA2 and H-Ras， which are regulated by microRNA let-7，were determined by RT-PCR. Results NF-κB p65 and Lin28B expression declined signifi-cantly after 48-h drug treatment（t=23.44，t=14.24；P<0.05）.Transcription levels of HMGA2 and H-Ras，which are related to self-renewal and multipotent differentiation of tumor cells，decreased 85%（P＜0.05） and 96%（P＜0.05），respectively，based on 2-△△Ct measurements. Conclusions Metformin at 16.56 g/L can effectively reduce NF-κB and Lin28B expression and inhibit HMGA2 and H-Ras transcrip-tion in MCF-7 cells.These findings suggest that metformin inhibits breast cancer at the cellular level.

Key words:  Breast neoplasms, Metformin, NF-κB p65, Lin28B, HMGA2, H-Ras