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. 2022 Sep 16;41:275. doi: 10.1186/s13046-022-02475-2

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© The Author(s) 2022

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. 5 — HGF/c-MET axis upregulates ETV1 via ERK1/2 activation. (A) The expression of ETV1 in PLC/PRF/5 cells treated with different concentrations of recombinant HGF. (B) The expression of ETV1 in HepG2 cells treated with different concentrations of HGF. (C) Relative luciferase activities of ETV1 promoter reporter vectors in indicated cells upon treatment with HGF. (D) Western blotting assays of ETV1, Akt, p-Akt, ERK1/2, p-ERK1/2, JNK, p-JNK, p38, p-p38, proceed with PI3K inhibitor (LY294002), ERK1/2 inhibitor (SCH772984), JNK inhibitor (SP600125), and p38 inhibitor (SB203580) upon HGF treatment in PLC/PRF/5 cells. (E) Relative luciferase reporter assays of PLC/PRF/5 cells transfected with serially truncated or mutant ETV1 promoter luciferase constructs treated with or without HGF. (F-H) The relative promoter luciferase activity, mRNA, and protein levels of ETV1 in the PLC/PRF/5 cells after transfection with shELK1 or control shRNA in the presence of HGF. (I) ChIP assays verified the direct binding of ELK1 to the ETV1 promoter in HCC cells. * Represented p < 0.05. All data were displayed as Mean ± SD