Epithelial-mesenchymal transition (EMT)

EMT is an essential developmental process implicated in cancer progression and metastasis.

EMT is defined by the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype with increased migratory and invasive behavior. These phenotypic changes are accompanied by the loss of intercellular adhesion (E-cadherin and occludins), down-regulation of epithelial makers (cytokeratins), up-regulation of mesenchymal markers (vimentin, fibronectin and smooth muscle actin), acquisition of fibroblast-like (spindle) morphology with cytoskeleton reorganization, and increase in motility, invasiveness and metastatic capabilities. The EMT is mediated, at least in part, by a number of specific transcription factors including Snail, Slug, SIP-1, yEF1, E12/24 and Twist, EMT is considered to be a powerful mechanism that facilitates cancer metastasis. Although EMT has been extensively investigated in the past few years, the mechanisms that regulate EMT in different breast carcinoma subtypes have not been fully explored. Current effort of Prof. Sima Lev and her research team is to Identify new regulators of EMT in breast cancer and thereby develop therapeutic strategies that prevent metastasis.

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