Objective To investigate the effect of icariin on epithelial-mesenchymal transition(EMT)of breast cancer cells and its possible mechanism.Methods Different concentrations of icariin were used to treat MDA-MB-231 cells.Scratch assay,Transwell assay,and qRT-PCR were used to sequentially detect cell invasion ability,miR-200c expression levels,and related protein expression changes.Results Compared with MCF-10A cells,miR-200c expression was significantly reduced in MCF-7,MDA-MB-231,and SK-BR-3 cells,with MDA-MB-231 cells showing the lowest expression(P<0.05).Icariin significantly inhibited the proliferation of MDA-MB-231 cells,and the cell inhibition rate increased significantly with increasing concentration.Compared with the control group and miR-200c NC group,the miR-200c inhibitor group and MDA-MB-231 cell healing rate increased,the number of transmembrane cells increased,the expression of β-catenin and Vimentin proteins increased,and the expression of miR-200c and E-cadherin proteins decreased(P<0.05).Compared with the control group,the icariin group showed a decrease in cell healing rate,a reduction in the number of transmembrane cells,a decrease in the expression of β-catenin and Vimentin proteins,and an increase in the expression of miR-200c and E-cadherin proteins(P<0.05).Compared with the icariin group,the icariin plus miR-200c inhibitor group showed an increase in cell healing rate,an increase in the number of transmembrane cells,an increase in β-catenin and Vimentin protein expression,and a decrease in miR-200c and E-cadherin protein expression(P<0.05).Conclusion Icariin can block the EMT process of breast cancer cells,inhibit the migration and invasion of tumor cells.its mechanism may be related to the upregulation of miR-200c expression and the regulation of the Wnt/β-catenin signaling pathway.
Breast cancerIcariinMigrationInvasionEpithelial-mesenchymal transitionmiR-200c
维普
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