期刊
CELL ADHESION & MIGRATION
卷 2, 期 4, 页码 249-251出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cam.2.4.6753
关键词
JAM-A; integrin; alpha(v)beta(3); FGF-2; breast cancer; cell migration and invasion; T47D; MDA-MB-231; siRNA
类别
资金
- National Institutes of Health [HL63960]
- National Center for Research Resources [1P20RR155801]
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.
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