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The epithelial to mesenchymal transition (EMT) is a dynamic and reversible process of transdifferentiation in which epithelial cells acquire characteristics typical of mesenchymal cells. During this transition, epithelial cells lose typical features such as cell–cell interactions (tight junctions, adherens junctions, desmosomes and gap junctions) and baso-apical polarity while acquiring cytosolic expansions, rear-front polarity, and increased migration/invasion capacity (1,2,4).

It is largely reported that EMT is regulated by various transcriptional factors such as Snail Family Transcriptional Repressor SNAIL1 and SNAIL2, zinc-finger E-box-binding (ZEB)1 and ZEB2 and TWIST transcription factors that suppress epithelial marker genes and activate genes related with the mesenchymal phenotype (4).

EMT is classified into three diverse subtypes: type-1 EMT, type-2 EMT and type-3 EMT. Type-1 EMT is involved in embryogenesis and organ development. Type-2 EMT is associated with wound healing, tissue regeneration and organ fibrosis. Type-3 EMT is implicated in cancer progression (4).

  (B) EMT is induced mainly by a set of transcription factors (EMT‐TFs) like ZEB1, ZEB2, SNAIL, SLUG and TWIST that differ in protein structure, size, and individual functions. All of them are repressors of epithelial factors like E‐cadherin and activate mesenchymal markers like Vimentin, Fibronectin or N‐cadherin. Epithelial cells displaying apical–basal polarity are held together by tight junctions, adherens junctions, and desmosomes and are anchored to the underlying basement membrane by hemidesmosomes. They express three different polarity complexes that together with the junctional molecules maintain epithelial cell polarity. In the classical EMT, expression of EMT‐TFs leads to inhibition of major components of these epithelial structures and concomitantly activates the expression of genes associated with the mesenchymal state. Cells gain front–rear polarity, display actin stress fibers, become motile and acquire invasive capacities. Notably, tumor cells very rarely switch to a completely mesenchymal phenotype, but fluently convert between various intermediate states displaying certain mesenchymal features but keeping partial sets of epithelial characteristics. Further, EMT is a reversible process. Mesenchymal cells can revert to the epithelial state undergoing MET. An important role in the execution of MET is played by microRNAs of the miR‐200 and mir‐34 families that are regulated in double‐negative feedback loops with the EMT‐TFs ZEB1/2 and SNAIL, respectively, that serve to reinforce either the epithelial or the mesenchymal state (5) .


EMT is not only a key element in embryonic development, organogenesis, and wound-healing, but it has been identified as a probable response to organ damage and a loss of functional epithelial cells, and it is involved in tumor progression, cancer cell invasion and in therapy resistance (breast, pancreas cancer ….) (2,3).
(1) Manfioletti G, Fedele M. Epithelial–Mesenchymal Transition (EMT) 2021. Int J Mol Sci. (2022);23(10):5848.
(2) Lachat C, et al. Epithelial to Mesenchymal Transition History: From Embryonic Development to Cancers. Biomolecules. (2021);11(6):782.
(3) Dudas J, et al. Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance. Cells. (2020);9(2):428.
(4) Marconi GD, et al. Epithelial-Mesenchymal Transition (EMT): The Type-2 EMT in Wound Healing, Tissue Regeneration and Organ Fibrosis. Cells. (2021);10(7):1587.
(5) Brabletz S, et al. Dynamic EMT: a multi‐tool for tumor progression. EMBO J. (2021);40(18):e108647.


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