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Betaig-h3 interacts with alpha3beta1 integrin to promote adhesion and migration of human hepatoma cells.

Abstract
betaig-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 3beta 1 integrin in human 7721 hepatoma cells. The addition of alpha 3beta 1 integrin antibodies inhibited the elevated adhesion and migration in beta ig-h3-over-expressing 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 3beta 1 integrin, beta ig-h3 activates FAK-paxillin signaling linkage, leads to cytoskeleton reorganization, and thus enhances the metastatic potentials of human hepatoma cells.
AuthorsJuan Tang, Ya-Mei Wu, Pu Zhao, Jian-Li Jiang, Zhi-Nan Chen
JournalExperimental biology and medicine (Maywood, N.J.) (Exp Biol Med (Maywood)) Vol. 234 Issue 1 Pg. 35-9 (Jan 2009) ISSN: 1535-3702 [Print] England
PMID18997105 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Extracellular Matrix Proteins
  • Integrin alpha3beta1
  • Paxillin
  • Transforming Growth Factor beta
  • betaIG-H3 protein
  • Focal Adhesion Kinase 1
  • PTK2 protein, human
Topics
  • Carcinoma, Hepatocellular (pathology, physiopathology)
  • Cell Adhesion
  • Cell Line, Tumor
  • Cell Movement
  • Cytoskeleton (pathology, ultrastructure)
  • Extracellular Matrix Proteins (genetics, metabolism)
  • Focal Adhesion Kinase 1 (genetics)
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Humans
  • Integrin alpha3beta1 (genetics, metabolism)
  • Liver Neoplasms (pathology, physiopathology)
  • Neoplasm Invasiveness
  • Paxillin (genetics)
  • Transfection
  • Transforming Growth Factor beta (genetics, metabolism)

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