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. 2023 May 31;22:90. doi: 10.1186/s12943-023-01793-z

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© The Author(s) 2023

Open Access This 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. 1 — EMT pathways are embedded in signalling networks in cancer cells. Various signalling pathways exemplified on the top promote EMT by activating EMT-TFs. A Transcriptional regulation of epithelial-mesenchymal plasticity. In cells undergoing EMT, EMT-TFs repress transcription of epithelial genes encoding components of various epithelial structures, such as polarity complexes and adherens junctions, and activate the expression of mesenchymal genes. MET-inducing transcription factors (MET-TFs) repress transcription of mesenchymal markers, activate epithelial transcription programs, and act in double-negative feedback loops involving EMT-TFs. B EMT-inducing signals are modified by EMT-TFs/microRNA loops. EMT-TFs and microRNAs form interrelated double-negative feedback loops which affect expression levels of certain components of EMT-inducing signalling network. C EMT-TFs physically interact with components of signalling pathways forming complexes that in turn influence target genes. D EMT/MET mutually regulate alternative splicing. EMT-TFs regulate expression of epithelial (e.g., ESRP1/2) or mesenchymal (e.g., QKI) splicing factors, which in turn determine formation of epithelial- or mesenchymal-specific protein isoforms required for the accomplishment of EMT or MET programs. E Expression of metabolic genes of glycolysis and oxidative phosphorylation pathways are controlled by EMT-TFs