miR-7对乳腺癌细胞阿霉素耐药性的逆转作用及机制  

Reverse offect of miR-7 on adriamycin resistance of breast cancer cells

作　　者：路选[1] 陈飞[1] 王颖[1] 李瑞青[1] 高小康[1] 孙鹤庆[1] 

机构地区：[1]扬州市第一人民医院,江苏扬州225000

出　　处：《山东医药》2016年第13期20-22,共3页Shandong Medical Journal

摘　　要：目的探讨microR(miR)-7对乳腺癌细胞阿霉素耐药性的逆转作用及可能的下游分子机制。方法采用ADR诱导体外人乳腺癌MCF-7细胞,建立阿霉素耐药性MCF-7/ADR细胞株;MCF-7或MCF-7/ADR乳腺癌细胞转染miR-7过表达载体(miR-7 mimic)或干扰miR-7载体(miR-7 inhibitor)48 h后,阿霉素(100 ng/m L)处理24h,MTT法测算细胞存活率;荧光定量PCR法测定miR-7和ABCC10 mRNA表达;蛋白免疫印迹法检测ABCC10蛋白表达。结果 MCF-7/ADR细胞表达低水平的miR-7和高水平的ABCC10。MCF-7/ADR过表达miR-7,ABCC10mRNA和蛋白表达受抑制,细胞的阿霉素敏感性增加,细胞活性下降;MCF-7低表达miR-7,ABCC10 mRNA和蛋白表达增加,细胞的阿霉素敏感性降低,而细胞活性增加。结论调控miR-7表达能逆转乳腺癌细胞阿霉素耐药性,其机制可能是miR-7通过调节ABCC10表达实现。Objective To investigate the reverse effect of microR（ miR）-7 on adriamycin resistance of breast cancer cells and its downstream molecule mechanism. Methods Human breast cancer MCF-7 cell line was exposed to gradually increasing density of adriamycin（ ADR） that was used to establish ADR-resistant MCF-7 / ADR cell line. MCF-7 or MCF-7 / ADR cells were transfected with miR-7 mimic or miR-7 inhibitor for 48 h. Then cells were exposed to ADR（ 100 ng /m L） for 24 h. MTT assay was used to evaluate cell survival,fluorescent quantitative PCR was used to determine miR-7 and ABCC10 mRNA expression and immunoblotting was used to determine ABCC10 protein expression. Results MCF-7 / ADR cell expressed lower level of miR-7 and high level of ABCC10. MiR-7 overexpression in MCF-7 / ADR cell inhibited ABCC10 mRNA and protein expression and enhanced ADR resistance thereby leading to the reduction of cell viability. In the contrary,silencing miR-7 in MCF-7 promoted ABCC10 mRNA and protein expression and increased cell viability. Conclusion Regulating MiR-7 expression may reverse the ADR resistance of breast cancer cells and its mechanism may be that miR-7 reverses ADR resistance by regulating ABCC10 expression.

关 键 词：乳腺癌 阿霉素 细胞活性 微小RNA-7 ABCC10蛋白 

分 类 号：R737.9[医药卫生—肿瘤]