Putting the brakes on cancer cell migration: JAM-A restrains integrin activation.
Junctional Adhesion Molecule A (JAM-A) is a member of the Ig superfamily of membrane proteins expressed in platelets, leukocytes, endothelial cells and epithelial cells. We have previously shown that in endothelial cells, JAM-A regulates basic fibroblast growth factor, (FGF-2)-induced angiogenesis via augmenting endothelial cell migration. Recently, we have revealed that in breast cancer cells, downregulation of JAM-A enhances cancer cell migration and invasion. Further, ectopic expression of JAM-A in highly metastatic MDA-MB-231 cells attenuates cell migration, and downregulation of JAM-A in low-metastatic T47D cells enhance migration. Interestingly, JAM-A expression is greatly diminished as breast cancer disease progresses. The molecular mechanism of this function of JAM-A is beyond its well-characterized barrier function at the tight junction. Our results point out that JAM-A differentially regulates migration of endothelial and cancer cells.
Naik
Ulhas P
UP
Department of Biological Sciences, Delaware Biotechnology Institute, University of Delaware, Newark, Delaware 19716, USA. unaik@udel.edu
Naik
Meghna U
MU
D000818:Animals; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002465:Cell Movement; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism*; D016023:Integrins / Q000378:metabolism*; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology*
D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; D016023:Integrins