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. Author manuscript; available in PMC: 2015 Oct 15.
Published in final edited form as: Nat Commun. 2015 Apr 15;6:6879. doi: 10.1038/ncomms7879

Figure 3. miR-1269a regulates EMT.

Figure 3

(a–c) Western blot (a), Immunofluorescence (b), and phase-contract images (c) of SW480 cells with a control vector (NC) or with ectopic miR-1269a expression (miR-1269a). Ectopic miR-1269a downregulated the epithelial marker E-cadherin, upregulated the mesenchymal markers N-cadherin and Vimentin, and changed cell morphology. (d–f) Immunofluorescence (d), Western blot (e), and phase-contract images (f) of SW620 cells with a control vector (Anti-NC) or with antisense RNA against endogenous miR-1269a (Anti-miR-1269a). SW620 cells are either untreated (d, upper panel) or treated with TGF-β1 (d, lower panel). miR-1269a knockdown suppressed TGF-β1 induction of EMT, as indicated by downregulation of N-cadherin and Vimentin, upregulation of E-cadeherin, and reversion from a mesenchymal-like morphology to an epithelial-like morphology. Scale bar, 15 µm.