Epithelial-mesenchymal transition (EMT) is a program of development of biological cells characterized by loss of cell adhesion, repression of E-cadherin expression, and increased cell mobility. EMT is essential for numerous developmental processes including mesoderm formation and neural tube formation.
Several oncogenic pathways (peptide growth factors, Src, Ras, Ets, integrin, Wnt/beta-catenin and Notch) induce EMT. In particular, Ras-MAPK has been shown to activate two related
transcription factors known as Snail and Slug. Both of these proteins are transcriptional repressors of E-cadherin and their expression induces EMT. Recently, activation of the phosphatidylinositol 3' kinase (PI3K)/AKT axis is emerging as a central feature of EMT.
Twist, another transcription factor, has also been shown to induce EMT, and is also implicated in the regulation of
metastasis. Expression of FOXC2, an important player during embryonic development has been shown to induce EMT and regulate metastasis. Moreover, expression of FOXC2 is induced when epithelial cellsundergo EMT by Snail, Twist, Goosecoid, and TGF-beta 1.
metastasisinvolves invasion, which has many phenotypic similarities to EMT, including a loss of cell-cell adhesion mediated by E-cadherin repression and an increase in cell mobility.
EMT is a characteristic feature of cells undergoing proliferation. Cells expanding in-vitro, like beta cells- and epithelial phenotype, of the pancreas, assume mesenchymal phenotype.
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