E-cadherin-mediated adhesion inhibits ligand-dependent activation of diverse receptor tyrosine kinases.

摘要: E-cadherin is an essential adhesion protein as well a tumor suppressor that silenced in many cancers. Its adhesion-dependent regulation of signaling has not been elucidated. We report can negatively regulate, manner, the ligand-dependent activation divergent classes receptor tyrosine kinases (RTKs), by inhibiting their association with decreases mobility and ligand-binding affinity. did regulate constitutively active mutant RTK (Neu*) or LPA receptors muscarinic receptors, which are two G protein-coupled receptors. EGFR was associated complex formation between depended on extracellular domain but independent β-catenin binding p120-catenin binding. Transfection conferred negative to human melanoma breast cancer lines downregulated endogenous E-cadherin. Abrogation may contribute frequent tumors.