Epithelial to Mesenchymal Transition
Epithelial to mesenchymal transition (EMT) is a biological process by which cells lose epithelial characteristics and acquire a migratory, mesenchymal phenotype. Epithelia are highly ordered monolayers of cells that often line tissues such as the intestine. Epithelial cells form a barrier to protect against pathogens and participate in secretion and absorption. In order to perform these functions, epithelial cells have apical-basal polarity and adhere tightly to each other via adherens and tight junctions. In contrast, mesenchymal cells differ in shape and display an increased capacity for migration and invasion. This phenotypic transition is centrally important to embryogenesis and can be induced by TGF-beta and Wnt signaling, which promote E-Cadherin transcriptional repression, Actin cytoskeleton rearrangement, and basement membrane remodeling. Molecular markers of epithelial to mesenchymal transition include increased expression of N-Cadherin and Vimentin, nuclear localization of beta-Catenin, and augmented levels of transcription factors that repress E-Cadherin expression. EMT is also involved in fibrosis during scar tissue development and may be pathologically relevant to the development of progressive fibrotic diseases. In addition, EMT and the reverse process, mesenchymal to epithelial transition (MET), are hypothesized to be involved in tumor cell intravasation and the formation of metastases.
- Actin Stress Fibers and Focal Adhesions During EMT
- Cell to Cell Adhesion Disassembly During EMT
- EMT Induction
- Epigenetics and EMT
- Epithelial Cell Markers and Intracellular Molecules
- Epithelial Cell Polarity
- Extracellular Matrix Remodeling and Cell Migration During EMT
- Mesenchymal Cells and EMT
- Mesenchymal to Epithelial Transition
- Negative Regulators of EMT