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The epithelial-to-mesenchymal transition pathway (EMT) is a fundamental cellular process in which epithelial cells lose their characteristic cell–cell adhesion, polarity, and stationary phenotype, and acquire mesenchymal properties including increased motility, invasiveness, resistance to apoptosis, and enhanced production of extracellular matrix proteins. EMT is essential for multiple physiological processes such as embryogenesis, organ development, and wound healing, and is aberrantly activated in pathological states including cancer metastasis and fibrosis. Key signaling pathways regulating EMT include transforming growth factor-beta (TGFb), Wnt/beta-catenin, Notch, and receptor tyrosine kinase pathways, which induce transcription factors such as SNAIL, ZEB, and Twist to repress epithelial marker genes (notably E-cadherin) and promote expression of mesenchymal markers (such as vimentin and N-cadherin). EMT is a complex, multi-step process and is reversible; the reverse is called mesenchymal-to-epithelial transition (MET).
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