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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Tamoxifen epigenetically modulates CXCL12 expression in MCF-7 breast cancer cells.
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Tamoxifen epigenetically modulates CXCL12 expression in MCF-7 breast cancer cells.

机译:他莫昔芬表观遗传学调控MCF-7乳腺癌细胞中的CXCL12表达。

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摘要

The CXCL12 chemokine binds to the CXCR4 receptor and contributes to survival, proliferation, and migration of malignant cells. Recent reports indicate that breast cancer cells lacking expression of CXCL12 but exhibiting CXCR4 can metastasize to target organs that secrete CXCL12. We observed that Tamoxifen (Tam), similarly to 5-dAzaC, results in significantly increased levels of CXCL12 transcript and protein in MCF-7 breast cancer cells. Bisulfite sequencing suggests that Tam, similarly to 5-dAzaC, may increase CXCL12 expression via reduction in methylation of cytosine in the cytosine-guanosine (CpG) dinucleotide island of the CXCL12 promoter of MCF-7 cells. Our results, together with findings of other researches, may suggest that Tam epigenetically activates CXCL12 expression in breast cancer cells and can make these cells less susceptible to attraction by exogenous CXCL12 to metastasis sites.
机译:CXCL12趋化因子与CXCR4受体结合,并有助于恶性细胞的存活,增殖和迁移。最近的报道表明,缺乏CXCL12表达但表现出CXCR4的乳腺癌细胞可以转移至分泌CXCL12的靶器官。我们观察到他莫昔芬(Tam)与5-dAzaC相似,导致MCF-7乳腺癌细胞中CXCL12转录本和蛋白质水平显着提高。亚硫酸氢盐测序表明,与5-dAzaC相似,Tam可通过减少MCF-7细胞CXCL12启动子的胞嘧啶-鸟苷(CpG)二核苷酸岛中胞嘧啶的甲基化来增加CXCL12表达。我们的结果,以及其他研究的发现,可能表明Tam表观遗传激活乳腺癌细胞中的CXCL12表达,并使这些细胞更不易被外源CXCL12吸引到转移部位。

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