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. 2023 Jan 24;16:6. doi: 10.1186/s13045-023-01398-5

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© The Author(s) 2023

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 — Protein degradation involved in EMT and cell stemness. Degradation of E-cadherin is regulated by E3 ligases RNF25, RNF43, and Hakai. Protein degradation of mesenchymal marker ZEB1 is mediated by E3 ligase SIAH1 and can be reversed by USP51. Snail is ubiquitinated by FBXO32 and deubiquitinated by USP1. For stemness sustaining pathways, β-TrCP participates in the ubiquitination of both YAP and β-catenin. In addition, STUB1 also facilitates the ubiquitination of YAP. USP10 facilitates deubiquitylation of YAP, and USP20, USP4, and USP22 deubiquitinate β-catenin