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Cell Adh Migr. 2008 Oct-Dec;2(4):249-51. Epub 2008 Oct 6.

Putting the brakes on cancer cell migration: JAM-A restrains integrin activation.

Author information

1
Department of Biological Sciences, Delaware Biotechnology Institute, University of Delaware, Newark, Delaware 19716, USA. unaik@udel.edu

Abstract

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.

PMID:
19262151
PMCID:
PMC2633686
[Indexed for MEDLINE]
Free PMC Article

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