epithelialtomesenchymal

Epithelial-to-mesenchymal transition (EMT) is a cellular program in which epithelial cells acquire mesenchymal traits, including increased motility and invasiveness, while losing polarity and stable cell–cell junctions. The term EMT is the conventional designation in the literature.

Molecular changes include downregulation of epithelial markers such as E-cadherin and cytokeratins, and upregulation of mesenchymal markers such as N-cadherin, vimentin, fibronectin, and α-smooth muscle actin. Key transcription factors driving EMT are Snail, Slug, ZEB1/2, and Twist1.

EMT is regulated by signaling networks including TGF-β, Wnt/β-catenin, Notch, and Hedgehog pathways, often integrated with hypoxia, inflammation, and mechanical cues. EMT also exists as a spectrum with partial or hybrid states, which can support collective migration and stem-like properties.

Developmental contexts include neural crest formation and organogenesis; EMT also contributes to wound healing and, in chronic injury, to organ fibrosis.

In cancer, EMT can promote invasion and metastasis and may contribute to resistance to therapy. However, its role is complex and not universal, with tumors often displaying varying EMT extents and sometimes reverting via mesenchymal-to-epithelial transition (MET) during colonization.

Assessment relies on marker analysis and transcriptomic profiling, including single-cell approaches that reveal heterogeneous EMT states. Therapeutic strategies targeting EMT face challenges due to cellular plasticity and potential effects on normal development and tissue repair.