Review
Version 2
Preserved in Portico This version is not peer-reviewed
Epithelial-Mesenchymal Transition: A Groundless Skyscraper
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Version 1
: Received: 29 February 2024 / Approved: 29 February 2024 / Online: 29 February 2024 (10:50:14 CET)
Version 2 : Received: 16 April 2024 / Approved: 16 April 2024 / Online: 16 April 2024 (15:50:00 CEST)
Version 2 : Received: 16 April 2024 / Approved: 16 April 2024 / Online: 16 April 2024 (15:50:00 CEST)
How to cite: Cao, Y. Epithelial-Mesenchymal Transition: A Groundless Skyscraper. Preprints 2024, 2024021729. https://doi.org/10.20944/preprints202402.1729.v2 Cao, Y. Epithelial-Mesenchymal Transition: A Groundless Skyscraper. Preprints 2024, 2024021729. https://doi.org/10.20944/preprints202402.1729.v2
Abstract
Epithelial–mesenchymal transition (EMT) is defined as a cellular process during which epithelial cells acquire mesenchymal phenotypes and behavior following the downregulation of epithelial features. EMT and its reversed process, the mesenchymal-epithelial transition (MET), and the special form of EMT, the endothelial-mesenchymal transition (EndMT), have been thought as a universal dogma controlling developmental and pathological processes. More than half a century of EMT study has made it a large research field and a mainstream concept. However, discrepancies and disputes over EMT and EMT research have also grown over time. Particularly, neither the epithelial and mesenchymal states/properties nor their regulatory networks nor specific markers have been defined, rendering the EMT, MET and EndMT concepts groundless. Moreover, EMT and MET effects should not be a cause, but rather a consequence of or an accompanying effect during developmental and pathological processes. EMT and MET represented by the change in cell shapes or adhesiveness or symbolized by EMT factors are biased interpretation of the overall change in cellular property and regulatory networks during development and cancer progression. The true meaning of EMT effects in some developmental and pathological processes, such as fibrosis, needs re-evaluation. But the core EMT factors are actually a few components of the regulatory networks of neural stemness, which determines tumorigenicity and pluripotency. The EMT effects in cancer progression and neural crest formation are wrong attribution of the role of neural stemness during cancer progression and the cell-intrinsic property of neural crest cells to the unknown mesenchymal state. It is time to reassess the significance of EMT and its related concepts in scientific research.
Keywords
epithelial–mesenchymal transition, mesenchymal-epithelial transition, endothelial-mesenchymal transition, epithelial state, mesenchymal state, controversy, developmental biology, fibrosis, cancer, neural stemness, tumorigenicity, pluripotency
Subject
Biology and Life Sciences, Cell and Developmental Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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