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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: miR-615-3p promotes the epithelial-mesenchymal transition and metastasis of breast cancer by targeting PICK1/TGFBRI axis

Fig. 2

miR-615-3p promotes breast cancer metastasis via EMT. a Transwell assay measuring MCF-7 cell migration (left panel) and invasion (right panel) with a control vector (NC) or with ectopic miR-615-3p expression. b Transwell assay measuring MDA-MB-231 cell migration (left panel) and invasion (right panel) with a control vector (Anti-NC) or with anti-miR-615-3p expression. c Representative images (left upper panel), H&E staining (left down panel), and the number of metastatic nodules (right panel) of lung metastasis. Ectopic miR-615-3p expression promoted lung metastasis of MCF-7 cells (left panel). Knockdown of endogenous miR-615-3p by antisense RNA suppressed lung metastasis of MDA-MB-231 cells (right panel). Western blot (d left panel) and immunofluorescence (e left panel)) of MCF-7 cells with a control vector (NC) or with ectopic miR-615-3p expression. Ectopic miR-615-3p down-regulated the epithelial marker E-cadherin, up-regulated the mesenchymal marker Vimentin. Western blot (d right panel) and immunofluorescence (e right panel) of MDA-MB-231 cells with a control vector (Anti-NC) or with antisense RNA against endogenous miR-615-3p (Anti-miR-615-3p). miR-615-3p knockdown suppressed induction of EMT, as indicated by downregulation of Vimentin and upregulation of E-cadherin. f The transfection efficiency of MCF-7(miR-615-p overexpression) and MDA-MB-231(anti-miR-615-p) was shown in the image

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