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The Epithelial–mesenchymal transition (EMT) pathway is a dynamic biological process in which epithelial cells lose their polarity and adhesion, acquiring mesenchymal characteristics such as enhanced migratory and invasive capacity, resistance to apoptosis, and increased ECM production. EMT is central to embryonic development, tissue repair, and regeneration, but aberrant activation of EMT is a key feature in the progression of cancer, metastasis, and tissue fibrosis. The pathway encompasses diverse signaling networks (such as TGF-β, Wnt, Notch, and receptor tyrosine kinases) and is regulated by master transcription factors, including Snail, Slug, Twist, and ZEB families. Therapeutic efforts focus on modulating these mediators to impact disease progression, particularly in oncology and fibrotic diseases
Drugs may - inhibit EMT-initiating growth factor receptors (TGF-βR, EGFR, FGFR, etc.) - block intracellular signal transduction (SMADs, β-catenin, MAPK, PI3K/Akt) - disrupt transcription factor activity (Snail, Slug, Twist, ZEB)
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