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作 者:韦达[1] 赵建华[1] 唐金海[1] 李秀娟[1] 陈志远[1]
出 处:《中国肿瘤外科杂志》2012年第1期34-37,共4页Chinese Journal of Surgical Oncology
摘 要:目的分析miRNA34a和miRNA200c在人乳腺癌细胞MCF-7和耐药株中的不同表达,探讨miRNA在乳腺癌MDR中的调节作用及其分子机制。方法以人乳腺癌细胞株MCF-7为亲本细胞,采用阿霉素(adriamycin,Adr)及多西紫杉醇(docetaxel,Doc)低浓度持续加量诱导法建立多药耐药的人乳腺癌细胞株MCF-7Adr及MCF-7Doc。应用real-timeRT-PCR法对miRNA检测并比较其在MCF-7和多药耐药细胞株MCF-7Adr及MCF-7Doc间的表达差异。结果 real-timeRT-PCR结果显示,miRNA200c的表达在MCF-7Adr及MCF-7Doc细胞中较MCF-7细胞中显著降低(均P<0.01);miRNA34a的表达在MCF-7Adr细胞中较MCF-7细胞中显著降低(P<0.01),在MCF-7Doc中两者无明显差异(P>0.05)。结论 miRNA在乳腺癌多药耐药细胞和其亲本细胞中有表达差异,可能参与了乳腺癌多药耐药的发生。Objective To analyze the difference of miRNAs( miRNA34a and miRNA200c) expression between human breast cancer MCF-7 cell lines and drug resistant cell lines to investigate the regulatory role of miRNAs in MDR breast cancer cells and the underlying mechanisms. Methods Two MDR breast cancer cell lines MCF-7Adr and MCF-7Doc were established respectively in vitro by gradually increasing the concentration of adfiamycin and docetaxel from tire parent cell line MCF-7. Real-time quantitative PCR was used to detect miRNAs in MCF-7 and MDR cell(MCF-7Adr and MCF-7 l)oc) amt compare their differences. Results Compared with their counterparts, real-time RT-PCR showed that rniRNA200c levels in MCF-TDoc and MCF-TAdr cells were down-regulated significantly, miRNA34a levels were down-regulated in MCF-7Adr and no differences in MCF-TDoc. Conclusions miRNAs are differentially expressed between muhidrug-resistant breast cancer cell line and its parental cell line, which suggest that miRNAs may play a role in the development of MDR in breast cancer cell.
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