miR-100抑制乳腺癌细胞迁移的作用和机制

目的:探究miR-100对乳腺癌细胞株MDA-MB-231迁移能力的调节与机制.方法:Real time-PCR检测人正常乳腺上皮细胞MCF-10A和乳腺癌细胞株MDA-MB-231中miR-100的基础表达水平.应用脂质体法将 miR-100 mimic及阴性对照分别转染乳腺癌细胞株MDA-MB-231,通过real time-PCR检测转染后miR-100的表达水平,细胞划痕实验检测过表达miR-100对MDA-MB-231细胞迁移能力的影响,Western blot方法检测slug、snail和E-cadherin等EMT蛋白表达水平的变化.结果:miR-100在乳腺癌细胞株MDA-MB-231中的表达明显低于人正常乳腺上皮细胞MCF-10A.转染miR-100 mimic的乳腺癌细胞株MDA-MB-231的miR-100表达水平明显增高,细胞划痕实验显示过表达miR-100的MDA-MB-231细胞划痕愈合速度明显减慢.过表达miR-100的MDA-MB-231细胞E-cadherin蛋白表达水平明显增加,而slug和snail蛋白表达水平明显降低.结论:miR-100抑制乳腺癌细胞株MDA-MB-231的迁移能力与其上调E-cadherin,下调slug、snail蛋白表达,抑制EMT有关.

The action and mechanisms of miR-100 on decreasing migration ability of breast cancer cells

Objective:To investigate the effects and mechanisms of miR-100 on the metastasis of breast cancer cell line MDA-MB-231.Methods:The expression of miR-100 in human normal breast epithelial cells MCF-10A and breast cancer cell line MDA-MB-231 were analyzed by real-time PCR.The expression of miR-100 was detected by real time-PCR after transfecting miR-100 mimic or the negative control into MDA-MB-231 breast cancer cell line.The cell migration ability of MDA-MB-231 cells after transfection were detected by cell scratch test.The expression of slug,snail and E-cadherin were detected by Western blot.Results:The expression of miR-100 in breast cancer cell line MDA-MB-231 was significantly lower than that in normal human breast epithelial cell line MCF-10A.The expression of miR-100 was significantly increased,cell scratches healing was significantly decreased,and the expression of E-cadherin protein was increased,while the expression of slug and snail protein was decreased in the MDA-MB-231 cells transfected with miR-100 mimic.Conclusion:miR-100 decreased the migration ability of breast cancer cells by inhibiting the EMT of the cells.