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. 2018 Feb 1;8:2097. doi: 10.1038/s41598-018-20146-1

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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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EPLIN and plectin regulate paxillin accumulation in RasV12-transformed cells surrounded by normal epithelial cells. (a–d) Effect of EPLIN-knockdown (a,b) or plectin-knockdown (c,d) on paxillin accumulation. MDCK-pTR GFP-RasV12 cells, MDCK-pTR GFP-RasV12 EPLIN-shRNA1 cells or MDCK-pTR GFP-RasV12 plectin-shRNA1 cells were mixed with normal MDCK cells on collagen gels. Cells were fixed after 16 h incubation with tetracycline and stained with anti-EPLIN (a) or anti-plectin (c) (red), and anti-paxillin (grey) antibodies and Hoechst (blue). Scale bars, 10 μM. (b,d) Quantification of (a,c). Data are mean ± SD from three independent experiments. (b) *P < 0.05, (d) *P < 0.0005; n ≧ 28 cells for each experimental condition. Values are expressed as a ratio relative to EPLIN-shRNA1 (-) (b) or plectin-shRNA1 (-) (d).