E-cadherin and Hakai: signalling, remodeling or destruction?
Salvatore Pece2
& J. Silvio Gutkind1
1
J. Silvio Gutkind is in the Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research and National Institutes of Health, Bethesda, Maryland 20892-4330, USA
sg39v@nih.gov
2
Salvatore Pece is in the Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy
Activation of tyrosine kinase receptors in epithelial cells results in the rapid disassembly of E-cadherin-mediated cell−cell adhesions. New research has identified Hakai, an E3-ubiquitin-ligase related to Cbl that binds E-cadherin in a tyrosine phosphorylation-dependent manner. By promoting the endocytosis and dynamic recycling or destruction of E-cadherin complexes, Hakai may control epithelial−mesenchymal transitions under physiological and pathological conditions.
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