Epithelial to Mesenchymal Transition

Epithelial to mesenchymal transition (EMT) is a biological process by which differentiated epithelial cells lose epithelial characteristics and acquire a migratory, mesenchymal phenotype. Although the intermediate stages of EMT have been challenging to capture and describe, the initiation and completion of EMT are better understood. Typically, epithelial cells display apical-basal polarity and adhere tightly to each other via tight and adherens junctions near the apical membrane and desmosomes in the basolateral membrane. The morphological changes that occur during EMT are induced by signal transduction pathways that reduce E-Cadherin expression, drive the disassembly of intercellular adhesion complexes, and promote Actin stress fiber and focal adhesion formation. These types of cellular changes result in the phenotypic transition to an elongated, mesenchymal cell that expresses extracellular matrix remodeling enzymes and has an increased capacity for migration and invasion. EMT and the reverse process, mesenchymal to epithelial transition (MET), are thought to be controlled by local cues within distinct microenvironments. For example, one model suggests that intraepithelial gamma delta T cells, which secrete cytokines, chemokines, and growth factors, regulate EMT/MET pathways in certain contexts. Overall, increasing evidence indicates that immune cell-dependent EMT/MET influences epithelial carcinogenesis progression in vivo.

EMT is a transient and reversible process that can be classified into three subtypes, depending on the biological and functional setting in which it occurs:

To learn more about research tools for EMT studies, please see our main EMT Research Topic Page. Click here to download a PDF (pdf 2 MB)