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胡清福, 许双塔, 许建华, 郑正荣, 吴飞敬, 赵清泉, 曾晓珊, 梁应辉. 雷公藤甲素对三阴性乳腺癌细胞BRCA1表达影响[J]. 中国公共卫生, 2018, 34(7): 1001-1003. DOI: 10.11847/zgggws1117335
引用本文: 胡清福, 许双塔, 许建华, 郑正荣, 吴飞敬, 赵清泉, 曾晓珊, 梁应辉. 雷公藤甲素对三阴性乳腺癌细胞BRCA1表达影响[J]. 中国公共卫生, 2018, 34(7): 1001-1003. DOI: 10.11847/zgggws1117335
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Qing-fu HU, Shuang-ta XU, Jian-hua XU, . Effect of triptolide on expression of BRCA1 in triple-negative breast cancer cells[J]. Chinese Journal of Public Health, 2018, 34(7): 1001-1003. DOI: 10.11847/zgggws1117335
Citation: Qing-fu HU, Shuang-ta XU, Jian-hua XU, . Effect of triptolide on expression of BRCA1 in triple-negative breast cancer cells[J]. Chinese Journal of Public Health, 2018, 34(7): 1001-1003. DOI: 10.11847/zgggws1117335
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雷公藤甲素对三阴性乳腺癌细胞BRCA1表达影响

Effect of triptolide on expression of BRCA1 in triple-negative breast cancer cells

    摘要
  • 摘要:
      目的  探讨雷公藤甲素（TPL）对三阴性乳腺癌细胞中乳腺癌易感基因1（BRCA1）表达影响及机制。
      方法  用不同浓度TPL（12.5、25.0、50.0和100.0 nmol/L）处理携带野生型BRCA1基因的三阴性乳腺癌细胞株MDA-MB-468后，采用噻唑蓝（MTT）法检测细胞增殖情况、RT-PCR法检测BRCA1、ATM（ataxia telangiectasia mutated）和ATR （ATM and Rad3-related）mRNA表达水平、Western blot检测BRCA1、ATM、ATR蛋白及BRCA1蛋白磷酸化表达水平。
      结果  不同浓度TPL处理后，MDA-MB-468细胞生长受到明显抑制，TPL 12.5、25.0、50.0、100.0 nmol/L剂量组MDA-MB-468细胞生长抑制率分别为13.3%、32.3%、42.9%、60.7%，抑制率与TPL呈浓度依赖性；与对照组比较，各剂量TPL组MDA-MB-468细胞BRCA1、ATM和ATR mRNA及蛋白表达水平均明显下调，呈剂量效应关系；TPL对MDA-MB-468细胞BRCA1中Ser-1524位点磷酸化作用具有明显抑制作用，并呈剂量效应关系。
      结论  雷公藤甲素可诱导三阴性乳腺癌细胞凋亡，其机制可能与其抑制细胞中BRCA1表达及其磷酸化水平有关。

     

    Abstract:
      Objective  To investigate the effect and mechanism of triptolide (TPL) on the expression of breast cancer susceptibility gene1 (BRCA1) in triple-negative breast cancer (TNBC) cells.
      Methods  TNBC cell line MDA-MB-468 carrying wild type BRCA1 gene was treated with different concentrations of TPL (12.5, 25, 50, and 100 nmol/L). The cell proliferation was detected with 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay; the expression of BRCA1, ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) mRNA were measured with real-time reverse transcription PCR (RT-PCR); and the expression of BRCA1 and its phosphorylation, ATM, and ATR protein were measured with Western blot.
      Results  The growth of MDA-MB-468 cells was significantly inhibited after treated with TPL and the inhibition rate was concentration-dependent, with the inhibition rate of 13.3%, 32.3%, 42.9%, and 60.7% for the cells treated with 12.5, 25.0, 50.0, and 100 nmol/L TPL. Compared to those of the control group, the expressions of BRCA1, ATM, and ATR mRNA and the expressions of BRCA1, ATM, and ATR protein were significantly reduced after treated with TPL and the reductions were also concentration-dependent. In addition, TPL inhibited specifically the phosphorylation of BRCA1Ser-152 in a dose-response manner.
      Conclusion  TPL could induct the apoptosis of triple-negative breast cancer cell line MDA-MB-468, and the possible mechanism is the inhibition of BRCA1gene expression and the phosphorylation of the gene.

     

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