Epithelial–mesenchymal transition process (EMT)

Epithelial–mesenchymal transition (EMT) is a reversible biological process in which epithelial cells lose their cell polarity and cell-cell adhesion properties and acquire migratory and invasive characteristics typical of mesenchymal cells. This transformation enables cells to detach from the primary tissue structure—losing apico-basal polarity and tight junctions—and become more motile by expressing proteins such as vimentin and N-cadherin instead of epithelial markers like E-cadherin. EMT plays essential roles in embryonic development—including gastrulation, neural crest migration, heart valve formation—as well as in adult processes like wound healing and organ fibrosis. In cancer biology, EMT facilitates tumor progression by enabling carcinoma cells to invade surrounding tissues, enter the bloodstream or lymphatic system, resist apoptosis/chemotherapy (“chemoresistance”), and establish secondary tumors at distant sites. The induction of EMT involves complex regulation through transcription factors such as SNAI/Snail family members, TWIST proteins, ZEB family members; these are activated downstream of signals including transforming growth factor beta (TGF-beta), fibroblast growth factor (FGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), hypoxia-inducible factors (HIFs) among others. The reverse process—mesenchymal-to-epithelial transition (MET)—also occurs during certain physiological events. Because EMT describes a cellular program rather than an individual molecule or receptor, it is not considered a canonical therapeutic “target” like an enzyme or receptor would be. Instead, therapies may aim to inhibit key drivers or regulators within the broader signaling networks that control this process. In summary: The “epithelial–mesenchymal transition process” refers to an important biological phenomenon with major implications for development and disease but does not represent an individual molecular drug target.

Other names

Epithelial-mesenchymal transitionEMTEpithelial to mesenchymal transition

Drugs do not directly target EMT as it is a biological process. Mechanisms include inhibition of signaling pathways that induce EMT, e.g., TGF-beta inhibitors.