Src-induced de-regulation of E-cadherin in colon cancer cells requires integrin signalling.

摘要: Although Src expression and activity are often elevated in colon cancer, the precise consequences of overexpression non-catalytic homology (SH) domains, or enhanced catalytic activity, unknown. We show that, KM12C cancer cells, causes components adherens junctions, including vinculin, to be redistributed Src-induced integrin adhesion complexes. Specifically, blocks proper assembly cell contacts after cells switched from media containing a low level calcium high calcium, E-cadherin remains internalized. In contrast, although domains is sufficient induce complexes, it does not disorganization E-cadherin-associated intercellular contacts. Surprisingly, disruption localization requires specific signalling, because redistribution blocked by loss cell-matrix interaction, inhibitory antibodies alpha(v) beta(1) subunits. Furthermore, phosphorylation integrin-regulated focal kinase (FAK) on Src-specific sites required for de-regulation E-cadherin, demonstrating interdependence between integrin-induced signals cadherin-associated changes induced Src.