microRNA-216a在乳腺癌中表达及对MCF-7细胞自噬的影响

目的 探讨microRNA-216a(miR-216a)在人乳腺癌组织中的表达情况,并探讨其对人乳腺癌细胞株MCF-7细胞自噬的影响和相关的分子机制。方法 应用实时定量RT-PCR方法检测30例乳腺癌组织和对应癌旁组织中miR-216a的相对表达量。进一步转染miR-216a抑制剂(AMO-216a)至MCF-7细胞中,应用qRT-PCR检测miR-216a的表达情况,采用MTT检测MCF-7细胞增殖情况,Western blot方法检测自噬相关蛋白Beclin 1的表达情况。结果 乳腺癌组织中miR-216a的表达水平明显增高;与对照组相比,转染AMO-216a后,MCF-7细胞中miR-216a水平明显降低,MCF-7细胞增殖被抑制,Beclin 1蛋白表达显著增加,差异具有统计学意义(P＜0.05)。结论 miR-216a在乳腺癌组织中表达增加,可能通过下调自噬相关蛋白Beclin 1表达来激活细胞自噬,促进乳腺癌的进展。

The expression of microRNA-216a in breast cancer and the effect on autophagy

Objective To investigate the expression of microRNA-216a(miR-216a)in patients suffering with breast cancer,and identify the function and mechanism of miR-216a on autophagy.Methods The expression of miR-216a in 30 tumor tissues and paired normal tissue of breast cancer were detected by qRT-PCR.Inhibiton of miR-216a in MCF-7 cell lines was done by transfection of miR-216a inhibitor(AMO-216a).Cell viability was detected by MTT assay.The level of Beclin 1 was detected by western blot.Results The level of miR-216a was significant elevated in tumor tissue.Cell viability was markedly decreased owing to inhibition of miR-216a in MCF-7 cells.The level of Beclin 1 was significantly increased by transfection of miR-216a inhibitor in MCF-7 cells(P＜0.05).Conclusion The level of miR-216a is increased in breast cancer tissue,and it might at least in part promote breast cancer via downregulating Beclin 1 and affecting autophagy.