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First published online March 5, 2008
doi: 10.1242/10.1242/jcs.000455
Commentary |
University of Nebraska Medical Center, Department of Oral Biology and Eppley Cancer Center, Omaha, NE 68198-7696, USA
* Author for correspondence (e-mail: mwheelock{at}unmc.edu)
Accepted 17 December 2007
The cadherin molecules at adherens junctions have multiple isoforms. Cadherin isoform switching (cadherin switching) occurs during normal developmental processes to allow cell types to segregate from one another. Tumor cells often recapitulate this activity and the result is an aggressive tumor cell that gains the ability to leave the site of the tumor and metastasize. At present, we understand some of the mechanisms that promote cadherin switching and some of the pathways downstream of this process that influence cell behavior. Specific cadherin family members influence growth-factor-receptor signaling and Rho GTPases to promote cell motility and invasion. In addition, p120-catenin probably plays multiple roles in cadherin switching, regulating Rho GTPases and stabilizing cadherins.
Key words: Cadherin, Biology, Switching
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