Figure 1.

Outline of a typical epithelial-mesenchymal transition EMT program. Cells undergoing EMT progressively lose typical epithelial cell-to-cell junctions, such as adherent and tight junctions, and the apical-basal polarity. At the same time, cells acquire a front-rear polarity, while gaining migratory and invasive abilities. Among epithelial markers, E-cadherin, a constituent of adherent junctions, is rapidly downregulated and is replaced by N-cadherin. This phenomenon is called ‘cadherin switch’. Similarly, epithelial intermediate filaments such as cytokeratins are replaced by mesenchymal counterparts, such as vimentin. Also, smooth muscle actin (α-SMA) is de novo induced. E-cadherin downregulation facilitates the activity of transcription factors relevant for the induction of the EMT program, such as nuclear factor kappa B subunit 1 (NF-κB) and β-catenin. Snail1, TWIST1, and ZEB1 are EMT-activating transcription factors which lead activation of EMT program.