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. 2018 Nov 26;38(13):2305–2319. doi: 10.1038/s41388-018-0577-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Inhibition of miR-508-3p in ovarian cancer cells is sufficient to induce mesenchymal phenotype. a Gene set enrichment analysis confirmed EMT-related programs are upregulated in miR-508-3p low expression group in TCGA. b Inverse phase microscopy (upper panel) and E-cadherin and vimentin staining (lower panels) of OV56 cells transfected with miR-508-3p inhibitor or control miRNA (miR-Ctrl) for 72 h. Cell nuclei were stained with DAPI. c The protein levels of E-cadherin and vimentin in OV56 cells transfected with miR-508-3p inhibitor or control miRNA (miR-Ctrl) for 72 h. β-actin was used as a control. d The mRNA levels of EMT genes between OV56 cells transfected with miR-508-3p inhibitor or control miRNA (miR-Ctrl) for 72 h. β-actin was used as a control. e Transwell chamber analysis of OV56 cells transfected with miR-508-3p inhibitor or control miRNA (miR-Ctrl) for 72 h. f Wound healing analysis of OV56 cells transfected with miR-508-3p inhibitor or control miRNA (miR-Ctrl) for 72 h. In all bar plots, p-values are based on two-tailed Student’s t-tests (*P < 0.05, **P < 0.01)