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. 2022 May 4;20:194. doi: 10.1186/s12967-022-03396-6

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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. 6 — Overexpression of CYP2E1 inhibits EMT in HCC cells. A Representative images of the morphological changes associated with EMT of MHCC-97H-CYP2E1, SMMC-7721-CYP2E1 and the respective control cells (×100). B Protein levels of EMT markers (E-cadherin, vimentin and N-cadherin) as well as EMT-related transcription factors (Twist, Slug and Snail) of the indicated cells detected by western blot. C Typical images of immunofluorescent staining for E-cadherin and vimentin in MHCC-97H and SMMC-7721 cells (×100). D Proposed model of the tumor suppressor role of CYP2E1 in HCC. Overexpression of CYP2E1 induces ROS accumulation and promotes the ubiquitin-mediated degradation of Dvl2, thereby, inhibiting the Wnt/β-catenin signaling and playing a suppressive role in HCC