Target intelligence / Profile preview

Epithelial–mesenchymal transition pathway (EMT pathway)

Target
EMT pathway
Molecular classification
Other (biological pathway/process)
01

Overview

The Epithelial–mesenchymal transition (EMT) pathway is a dynamic biological process in which epithelial cells lose their polarity and adhesion, acquiring mesenchymal characteristics such as enhanced migratory and invasive capacity, resistance to apoptosis, and increased ECM production. EMT is central to embryonic development, tissue repair, and regeneration, but aberrant activation of EMT is a key feature in the progression of cancer, metastasis, and tissue fibrosis. The pathway encompasses diverse signaling networks (such as TGF-β, Wnt, Notch, and receptor tyrosine kinases) and is regulated by master transcription factors, including Snail, Slug, Twist, and ZEB families. Therapeutic efforts focus on modulating these mediators to impact disease progression, particularly in oncology and fibrotic diseases

Other names
Epithelial-mesenchymal transitionEMTepithelial to mesenchymal transitionMET (refers to the reverse process, mesenchymal-epithelial transition)
02

Mechanism of action

Drugs may - inhibit EMT-initiating growth factor receptors (TGF-βR, EGFR, FGFR, etc.) - block intracellular signal transduction (SMADs, β-catenin, MAPK, PI3K/Akt) - disrupt transcription factor activity (Snail, Slug, Twist, ZEB)

03

Biological functions

Embryonic developmentTissue repair and regenerationCell migration and invasionStem cell plasticity/reprogrammingOrgan fibrosisCancer progression and metastasis
04

Disease associations

Cancer (metastasis, invasion, progression)Organ fibrosisWound healing disordersDevelopmental disorders
05

Safety considerations

Targeting EMT may impair normal developmental and tissue repair processesOff-target effects due to pathway involvement in many physiological settingsPotential for tissue toxicity and wound healing complications
06

Interacting drugs

Transforming growth factor-β (TGF-β) inhibitors (e.g., galunisertib)

4 more in the full profile.

07

Biomarkers

Downregulation of E-cadherin (CDH1)Upregulation of N-cadherin, vimentin, fibronectinExpression of EMT transcription factors (Snail, Slug, Twist, ZEB1/2)

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