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. 2017 Jun 16;7:3709. doi: 10.1038/s41598-017-04011-1

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© The Author(s) 2017

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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FOXK1 regulates EMT in vitro. (A) Morphology of pooled stable transfectants of Vector, RUFY3, and RUFY3-FOXK1 siRNA, as visualized under a phase-contrast microscope. (B) Immunofluorescence and microscopic visualization of E-cadherin (red) and vimentin (green) staining in RUFY3-scr-siRNA and RUFY3-FOXK1-siRNA cells. (C) The EMT biomarkers, including E-cadherin, vimentin, MMP2 and MMP9, were detected by western blot. (D) Western blot analyses of pooled stable transfectants with vector and RUFY3, examining p-ERK and p-Akt expression in LoVo cells treated with U0126 or LY294002. (E) Decreased FOXK1 expression inhibited the AKT/ERK/EMT signaling pathway, as detected using western blot analysis. Scale bars represent 50 μm in (A) and 20 μm in (B). The results were reproduced in three independent experiments. The full-length blots/gels are presented in Supplementary Figure 9.