Adherens junctions (AJs) are molecular complexes that mediate cell-cell adhesive interactions and play pivotal roles in maintenance of tissue organization in adult organisms and at various stages of development. AJs consist of cadherin adhesion receptors, providing homophilic ligation with cadherins on adjacent cells, and members of the catenin protein family: p120, β- and α-catenin. α-catenin's linkage with the actin cytoskeleton defines the linear or punctate organization of AJs in different cell types. Myosin II-dependent tension drives vinculin recruitment by α-catenin and stabilizes the linkage of the cadherin/catenin complex to F-actin. Neoplastic transformation leads to prominent changes in the organization, regulation and stability of AJs. Epithelial-mesenchymal transition (EMT) whereby epithelial cells lose stable cell-cell adhesion, and reorganize their cytoskeleton to acquire migratory activity, plays the central role in cancer cell invasion and metastasis. Recent data demonstrated that a partial EMT resulting in a hybrid epithelial/mesenchymal phenotype with retention of E-cadherin is essential for cancer cell dissemination. E-cadherin and E-cadherin-based AJs are required for collective invasion and migration, survival in circulation, and metastatic outgrowth.

E-cadherin is the main component of epithelial adherens junctions (AJs), which play a crucial role in the maintenance of stable cell–cell adhesion and overall tissue integrity. Down-regulation of E-cadherin expression has been found in many carcinomas, and loss of E-cadherin is generally associated with poor prognosis in patients. During the last decade, however, numerous studies have shown that E-cadherin is essential for several aspects of cancer cell biology that contribute to cancer progression, most importantly, active cell migration. In this review, we summarize the available data about the input of E-cadherin in cancer progression, focusing on the latest advances in the research of the various roles E-cadherin-based AJs play in cancer cell dissemination. The review also touches upon the “cadherin switching” in cancer cells where N- or P-cadherin replace or are co-expressed with E-cadherin and its influence on the migratory properties of cancer cells.

Epithelial–mesenchymal transition (EMT) is a fundamental process of morphogenesis whereby epithelial cells acquire the mesenchymal phenotype. Multiple data suggest a critical role of EMT in tumor...