Several molecular mechanisms contribute directly and mechanically to the loss of epithelial phenotype. During epithelial-mesenchymal transition (EMT), adherens junctions and desmosomes are at least partially dissociated. At the same time, a massive cytoskeleton reorganization takes place, involving the rho family and the remodeling of the actin microfilament mesh. Numerous pathways have been described in vitro that control phenotype transition in specific cell models. In vivo developmental studies suggest that transcriptional control, activated by a specific pathway involving Ras, Src and potentially the Writ pathway, is an essential step, Recent functional and localization experiments indicate that the slug/snail family of transcription factors functions overall as an epithelial phenotype repressor and could represent a key EMT contributor. (C) 2001 John Wiley & Sons, Inc.
Leaving the neighborhood: molecular mechanisms involved during epithelial-mesenchymal transition
2001-10 / vol 23 / pages 912-923
protein-kinase-c; beta-catenin; bladder-carcinoma cells; cell-cell adhesion; e-cadherin gene; extracellular-matrix; factor snail; finger transcription factor; neural crest; src family kinases