Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells lose polarity and cell-cell adhesion to gain migratory, mesenchymal-like properties; the reverse process is mesenchymal-to-epithelial transition (MET).
Between these two extremes lies partial EMT (p-EMT), a hybrid state — associated with DNA-hypomethylated stemness genes — that lets tumor cells retain some epithelial adhesion while migrating collectively as clusters, then rapidly undergo MET to re-establish epithelial identity at a distant metastatic site.
Tumor hypoxia is one well-established trigger of EMT programs: TGF-β signaling activated under hypoxic stress can drive tumor and stromal cells toward an EMT-like, extracellular-matrix-remodeling state that favors invasion and metastatic spread.
Related terms
Source papers
- Circulating Tumor Cells in the Blood Microenvironment: Survival Mechanisms and Metastatic Potential doi:10.1186/s44424-026-00056-0
- Hypoxia shapes both therapeutic response and resistance in metastatic clear cell renal cell carcinoma doi:10.1016/j.ccell.2026.05.007