Epithelial-Mesenchymal Transition (EMT)
Cellular program converting epithelial cells to motile mesenchymal phenotype.
Overview
EMT is a reversible process in which epithelial cells lose cell-cell adhesion (E-cadherin downregulation), apical-basal polarity, and gain mesenchymal markers (N-cadherin, vimentin, fibronectin) and migratory capacity. EMT transcription factors (Snail, Slug, Twist, ZEB1/2) are activated by TGF-β, Wnt, Notch, and growth factor signaling. EMT is essential for gastrulation, neural crest migration, and wound healing but is reactivated in cancer metastasis.
Cellular Location
Epithelial tissues
Clinical Significance
Critical for embryonic development; hijacked in cancer metastasis; associated with chemoresistance and cancer stem cell properties; therapeutic target for metastasis prevention.
Key Molecules
Key Enzymes
Related Pathways
TGF-β/BMP Signaling
Multifunctional cytokine signaling controlling growth, differentiation, and immune regulation.
Wnt/β-Catenin Pathway
Controls cell fate, proliferation, and polarity through β-catenin stabilization.
Notch Signaling Pathway
Juxtacrine signaling controlling cell fate decisions via proteolytic receptor activation.