Epithelial-mesenchymal transition.
Journal
Cell
Journal Volume
188
Journal Issue
20
Start Page
5436
End Page
5486
ISSN
1097-4172
Date Issued
2025-10-02
Author(s)
Abstract
Epithelial-mesenchymal transition (EMT) is a fundamental mechanism involved in the morphogenesis of metazoans. Through this evolutionarily conserved multi-stage process, cells acquire quasi-epithelial to multiple intermediate morphologies with epithelial and mesenchymal attributes, rarely reaching a complete mesenchymal phenotype. Complex evolutionary-conserved morphogenetic movements in gastrulation are described extensively, as they exemplify the extent of epithelial cell plasticity in the animal kingdom. Nonetheless, a single-gene knockout can modify the mode of gastrulation while achieving the same body plan. Numerous interconnected mechanisms drive different degrees of EMT, including surface receptor signaling, metabolism, and epigenetics. EMT is reactivated in adult tissues during repair and disease, particularly in cancer initiation, progression to metastasis, and refractoriness to treatment. EMT also contributes to dormancy and drug tolerance, leading to minimal residual disease at the origin of recurrences. Multiple EMT states coexist in tumors, creating a dynamic ecosystem for generating an inflammatory microenvironment, stemness, invasion, and metastasis. This review provides an in-depth description of these aspects along with recent controversies and offers new opportunities to further explore the multiple functions of EMT. Examining the potential attributes of EMT in tissue repair, fibrosis, and cancer progression can provide new opportunities for therapeutic intervention.
Subjects
carcinoma
epithelial-mesenchymal transition
fibrosis
gastrulation
initiation
metazoans
minimal residual disease
progression
recurrences
resistance
therapies
wound healing
SDGs
Type
review article