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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. 2 — TGF-β and EGF could induced EMT in HCEs. a A combination of TGF-β 10 nM and EGF (20 nM) could induced HCEs to show an EMT phenotype. b–d The changes in EMT markers were detected with qRT-PCR, western blot and immunofluorescence (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). e, f Cell migration in HCEs induced by TGF-β (10 nM) and EGF (20 nM). Cell migration was determined by the wound healing assay and transwell assay (*p < 0.05, ***p < 0.001). g Apoptosis in HCEs induced by TGF-β (10 nM) and EGF (20 nM). The apoptosis cells were decreased compared with the HCEs without inducement (*p < 0.05)