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Global communication by the epithelial cell layer is maintained through gap junctional complexes, separated from adjacent tissues by a basal lamina. Mesenchymal cells are loosely organized in a three-dimensional extracellular matrix, comprising connective tissue adjacent to the stroma. Conversion of epithelial cells to mesenhymal cells involves profound phenotypic changes, including loss of cell-cell adhesion, loss of cell polarity, and the acquisition of migratory and invasive properties (1). The process of epithelial-mesenchymal transition (EMT) is a critical event during embryonic development, required for morphogenetic movements during gastrulation and organ formation, but also a convenient venue for epithelial-derived tumors to become invasive and rapidly metastasize (2, 3). EMT endows cells with migratory and invasive properties, induces stem cell properties, and prevents apoptosis and senescence, thus orchestrating the initiation of metastasis (3, 4). Loss of epithelial-cell markers (E-cadherin, β-catenin) and gain of mesenchymal-cell markers (N-cadherin, vimentin), at the leading edge or invasive front of solid tumors, is associated with progression to metastasis (3). To preserve cellular shape and polarity, the intracellular domains of cadherins connect to the actin cytoskeleton through α-catenin and β-catenin. It is the signaling activities of mesenchymal cells that facilitate migration and survival in an anchorage-independent environment (2, 3). Thus even if there is no histological evidence of cellular intermediates during the transition, activation of mesenchymal genes in epithelial cells is critical for EMT success. The contribution of a tumor-suppressor gene’s activity to EMT is a fresh determinant in the EMT landscape. In this issue of PNAS, Xie et al. (5) report a unique player in the mechanistic control of …

ASK-ing EMT not to spread cancer