Cancer-associated fibroblasts (CAFs) promote tumour invasion and metastasis. We show
that CAFs exert a physical force on cancer cells that enables their collective invasion. Force …

We have previously shown that the switch from N-cadherin to OB-cadherin expression
increases intercellular adhesion between fibroblasts during their transition from a migratory …

The loss of E‐cadherin expression or function in epithelial carcinomas has long been
thought as a primary reason for disruption of tight epithelial cell‐cell contacts and release of …

E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic
cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells …

The loss of E-cadherin expression in association with the epithelial–mesenchymal transition
(EMT) occurs frequently during tumor metastasis. However, metastases often retain E …

E-cadherin plays a key role at adherens junctions between epithelial cells, but the
mechanisms controlling its assembly, maintenance, and dissociation from junctions remain …

During epithelial morphogenesis, E-cadherin adhesive junctions play an important part in
mechanically coupling the contractile cortices of cells together, thereby distributing the …

Cancer cells that originate from epithelial tissues typically lose epithelial specific cell–cell
junctions, but these transformed cells are not devoid of cell–cell adhesion proteins. Using …

Classical cadherins are the key molecules that control cell–cell adhesion. Notwithstanding
this function, it is also clear that classical cadherins are more than just the “glue” that keeps …

Plasticity of cancer invasion and metastasis depends on the ability of cancer cells to switch
between collective and single-cell dissemination, controlled by cadherin-mediated cell–cell …