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. 2016 Jan 9;7(25):37524–37535. doi: 10.18632/oncotarget.6852

Figure 2. Restoration of miR-101 expression inhibits EMT and promotes the sensitivity of NSCLC cells to cisplatin in vitro.

Figure 2

A. The IC50 for cisplatin of A549-res and NCI-H520-res cells transfected with miR-101 mimics was significantly lower than for cells transfected with miR-control. B. The cisplatin IC50 values of A549-res and NCI-H520-res cells transfected with anti-miR-101 mimics were higher than for cells transfected with anti-miR-control. C. The apoptosis rates of A549-res and NCI-H520-res cells transfected with miR-101 mimics were higher than those of cells transfected with miR-control. D. The apoptosis rates of A549-res and NCI-H520-res cells transfected with anti-miR-101 mimics were lower than those of cells transfected with anti-miR-control. E. Transwell migration assays and Matrigel invasion assays showed that restoration of miR-101 expression inhibited migration and invasion abilities of A549-res and NCI-H520-res cells and that anti-miR-101 overexpression promoted those abilities. F. Immunofluorescence assays in A549-res cells revealed that miR-101 overexpression dramatically promoted the expression of epithelial markers (E-cadherin and α-catenin) and dramatically suppressed the expression of mesenchymal markers (vimentin and N-cadherin). G. Western blotting assays showed that restoration of miR-101 expression significantly increased the expressions of epithelial markers and significantly inhibited the expressions of mesenchymal markers.