Retooling of the β4 Integrin in Tumor Cells—Ligands Lost and Kinase Gained

AbstractIn carcinoma cells, the β4 integrin functions in a ligand-independent manner to promote proliferation, migration, and invasion. An interesting new paper (Trusolino et al., 2001) describes a mechanism whereby the β4 integrin cytoplasmic tail becomes an integrin ligand-independent adaptor protein for the Met receptor tyrosine kinase, thereby enhancing the mitogenic, morphogenic, and motogenic properties of Met