Journal
EXPERIMENTAL BIOLOGY AND MEDICINE
Volume 234, Issue 1, Pages 35-39Publisher
SAGE PUBLICATIONS LTD
DOI: 10.3181/0806-RM-187
Keywords
beta ig-h3; hepatoma cells; metastasis; signal pathway; alpha 3 beta 1 integrin
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Funding
- National Natural Science Foundation of China [30771119, 30530720]
- National Basic Research,aid Development Program of China [2006CB709504]
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beta ig-h3 is a TGF-induced extracellular matrix (ECM) protein. Our previous evidence suggests that beta ig-h3 may promote adhesion and invasion potential of human hepatoma cells, but the mechanism underlying this process is still unknown. The present study identifies a pivotal role for molecules of the beta ig-h3 signal transduction pathway. We demonstrated that beta ig-h3 co-immunoprecipitated with alpha 3 beta 1 integrin in human 7721 hepatoma cells. The addition of alpha 3 beta 1 integrin antibodies inhibited the elevated adhesion and migration in beta ig-h3-overexpressing 7721 cells, but not in beta ig-h3 siRNA transfected 7721 cells. The expression and activity of integrin downstream molecules FAK and paxillin show a positive correlation with beta ig-h3 expression in different human hepatoma cells. Levels of focal adhesions and stress fibers were decreased in beta ig-h3 siRNA transfected 7721 cells. We suggest that by interaction with alpha 3 beta 1 integrin, beta ig-h3 activates FAK-paxillin signaling linkage, leads to cytoskeleton reorganization, and thus enhances the metastatic potentials of human hepatoma cells. Exp Biol Med 234:35-39, 2009
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