EMT: when epithelial cells decide to become mesenchymal-like cells.

By Raghu Kalluri. Journal of Clinical Investigation, 2009

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Coexpression of Oct4 and Nanog enhances malignancy in lung adenocarcinoma by inducing cancer stem cell-like properties and epithelial-mesenchymal transdifferentiation. (2010, background): “Intensive studies revealed that transcriptional factors, such as Snail, Slug, and Twist, regulate EMT process (21, 22).”
Rac and Rho GTPases in cancer cell motility control (2010, background): “The transcriptional programme leads to regulation of a series of proteins: decrease of E-cadherin for disruption of adherens junctions, increase in N-cadherin and Met proto-oncogene to drive motility, as well as increase in MMPs and uPA/uPAR proteolytic systems to degrade 3 D barriers [71,72].”
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “Unlike types I and II which perform necessary physiologic functions, type III is a pathophysiologic adaptation of the process, and is closely associated with progression of neoplasia occurring in cells containing certain epigenetic and genetic changes [4, 19].”
Cancer as a metabolic disease (2010, background): “The epithelial-mesenchymal transition (EMT) posits that metastatic cells arise from epithelial cells through a step-wise accumulation of gene mutations that eventually transform an epithelial cell into a tumor cell with mesenchymal features [6,100,194-196].”