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三氧化二砷对乳腺癌细胞MDA-MB-231雌激素受体α的去甲基化作用[J]. 肿瘤防治研究, 2011, 38(07): 749-751. DOI: 10.3971/j.issn.1000-8578.2011.07.005
引用本文: 三氧化二砷对乳腺癌细胞MDA-MB-231雌激素受体α的去甲基化作用[J]. 肿瘤防治研究, 2011, 38(07): 749-751. DOI: 10.3971/j.issn.1000-8578.2011.07.005
Demethylation of Estrogen Receptor-α in Breast Cancer Cells MDA-MB-231 after Treated by Arsenic Trioxide[J]. Cancer Research on Prevention and Treatment, 2011, 38(07): 749-751. DOI: 10.3971/j.issn.1000-8578.2011.07.005
Citation: Demethylation of Estrogen Receptor-α in Breast Cancer Cells MDA-MB-231 after Treated by Arsenic Trioxide[J]. Cancer Research on Prevention and Treatment, 2011, 38(07): 749-751. DOI: 10.3971/j.issn.1000-8578.2011.07.005

三氧化二砷对乳腺癌细胞MDA-MB-231雌激素受体α的去甲基化作用

Demethylation of Estrogen Receptor-α in Breast Cancer Cells MDA-MB-231 after Treated by Arsenic Trioxide

  • 摘要: 目的研究三氧化二砷(As2O3)作用于乳腺癌细胞MDA-MB-231后,对雌激素受体α(ERα)表达的影响,并初步探讨其机制。方法用As2O3处理ERα阴性的人乳腺癌细胞MDA-MB-231,甲基化特异性PCR (MSP)检测ERα启动子CpG岛的甲基化状态,反转录PCR(RT-PCR)检测ERα mRNA表达水平的变化。以雌激素受体α阳性的人乳腺癌细胞MCF-7 为阳性对照。结果MDA-MB-231细胞ERα启动子CpG岛存在高甲基化,经过As2O3处理后,CpG岛高甲基化水平降低,ERα mRNA恢复表达。结论 一定浓度的As2O3能够使人乳腺癌细胞MDA-MB-231 ERα启动子中的CpG岛发生去甲基化,重新恢复mRNA的表达。

     

    Abstract: ObjectiveTo study the expression of Estrogen receptor-α(ERα) after treatment with different concentration of arsenic trioxide in breast cancer cells MDA-MB-231, and explore its mechanism. MethodsERα negative human breast cancer cells MDA-MB-231 were treated by arsenic trioxide, methylation-specific PCR (MSP) was used to detect the methylation status of CpG island of the promoter of ERα gene, reverse transcriptase PCR (RT-PCR) was used to detect the expression level of ERα mRNA. The ERα-positive human breast cancer cells MCF-7 was used as the positive control. ResultsThe CpG island of the promoter of ERα was hypermethylation in MDA-MB-231 cells, CpG island was demethylated and ERα mRNA expression was restored after treatment by As2O3. ConclusionCertain concentration of As2O3 can demethylate the CpG island of the promoter of ERα in breast cancer cells MDA-MB-231 and restores its mRNA expression.

     

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