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. 2020 Sep 1;18:332. doi: 10.1186/s12967-020-02499-2

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Downregulating DUSP5 or MAP3K11could promote HCEs migration and EMT. a, b The shRNAs which had the best knockdown efficiency were selected with qRT-PCR. c, d The effect of pCMV-myc-DUSP5, pCMV-myc-MAP3K11, DUSP5-shRNA2# and MAP3K11-shRNA#1. HCEs were transfected with pCMV-myc and scr as control. e Cell migration was determined by the wound healing assay (**p < 0.01). f Cell migration was determined by the transwell assay (**p < 0.01). g, h The changes in EMT markers, after HCEs were transfected with pCMV-myc-DUSP5, pCMV-myc-MAP3K11, pCMV-myc, DUSP5-shRNA2#, MAP3K11-shRNA#1 and shRNA control. (*p < 0.05, **p < 0.01, ***p < 0.001)