Epithelial-mesenchymal transition pathway (EMT pathway)

Epithelial-mesenchymal transition (EMT) pathway describes a cellular program, not a discrete molecule, in which epithelial cells lose cell-cell adhesion and polarity, acquiring mesenchymal traits such as increased motility and invasiveness[1][4][7]. EMT is regulated by multiple signaling networks—including TGF-β, Wnt/β-catenin, Notch, PI3K/AKT/mTOR, RAS/RAF/MEK/ERK, and growth factor receptors—which activate key transcription factors like Snail, Slug, ZEB1/2, and Twist[3][5][6][7][9]. Physiologically, EMT is crucial for embryonic morphogenesis and tissue repair; pathologically, it drives metastasis and therapy resistance in cancer and contributes to organ fibrosis[3][6][8]. The EMT pathway is a concept encompassing myriad molecular actors and regulatory circuits, not a single therapeutic target; drug discovery efforts focus on inhibiting or reversing EMT by targeting its upstream regulators or downstream effectors[2][8][5]. EMT state is often monitored by loss of epithelial biomarkers (e.g., E-cadherin) and gain of mesenchymal markers (e.g., vimentin, N-cadherin)[7][1][4]. Because the “EMT pathway” is not a discrete protein, receptor, enzyme, or single gene entity, but rather a cell-state program, it is not conventionally classed as a direct drug target, and there are currently no approved drugs that "directly" target EMT itself—rather, drugs modulating EMT exist for specific components (TGF-β inhibitors, Wnt pathway modulators, etc.)[2][8][5].\n\nFurther notes: \n- is_incorrect is marked "true" because "Epithelial-mesenchymal transition pathway" is not a molecule, receptor, or classically defined drug target, but a complex biological process/pathway[7][2][8]. \n- Many anti-cancer strategies seek to "target EMT" by inhibiting inducers such as TGF-β, Wnt/β-catenin, Notch, EGFR, or related pathways[2][5][8]. Examples include TGF-β inhibitors, Wnt pathway modulators, and various small molecule or antibody drugs, but these act upstream or on effectors—not the EMT process as a unique molecular target. \n- Biomarkers for monitoring EMT include both transcription factors and surface/cytoskeletal proteins[7][1]. \n- Safety concerns and mechanisms of action are attributed to the specific molecules targeted, not the EMT program as a whole.\n\nFor canonical targets, best practice is to specify an individual molecule or factor in the EMT pathway (such as "Transforming growth factor beta receptor 1" or "Snail family transcriptional repressor 1").

Other names

EMTEpithelial to mesenchymal transitionEpithelial-mesenchymal transitionEpithelial to mesenchymal transition pathway

None (see note below; drugs target inducing/inhibiting pathways, not EMT as a molecule)