ZFIN ID: ZDB-PUB-061020-46
Galectin-1 is essential in tumor angiogenesis and is a target for antiangiogenesis therapy
Thijssen, V.L., Postel, R., Brandwijk, R.J., Dings, R.P., Nesmelova, I., Satijn, S., Verhofstad, N., Nakabeppu, Y., Baum, L.G., Bakkers, J., Mayo, K.H.,Poirier, F., and Griffioen, A.W.
Date: 2006
Source: Proceedings of the National Academy of Sciences of the United States of America   103(43): 15975-15980 (Journal)
Registered Authors: Bakkers, Jeroen, Postel, Ruben
Keywords: none
MeSH Terms:
  • Animals
  • Cell Movement
  • Cell Proliferation
  • Cells, Cultured
  • Disease Progression
  • Endothelial Cells/metabolism
  • Endothelial Cells/pathology
  • Galectin 1/deficiency
  • Galectin 1/genetics
  • Galectin 1/metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • Mice, Knockout
  • Neoplasm Transplantation
  • Neoplasms/blood supply*
  • Neoplasms/genetics
  • Neoplasms/metabolism*
  • Neoplasms/therapy
  • Protein Binding
  • Proteins/metabolism
  • Zebrafish
PubMed: 17043243 Full text @ Proc. Natl. Acad. Sci. USA
FIGURES
ABSTRACT
We describe that galectin-1 (gal-1) is a receptor for the angiogenesis inhibitor anginex, and that the protein is crucial for tumor angiogenesis. gal-1 is overexpressed in endothelial cells of different human tumors. Expression knockdown in cultured endothelial cells inhibits cell proliferation and migration. The importance of gal-1 in angiogenesis is illustrated in the zebrafish model, where expression knockdown results in impaired vascular guidance and growth of dysfunctional vessels. The role of gal-1 in tumor angiogenesis is demonstrated in gal-1-null mice, in which tumor growth is markedly impaired because of insufficient tumor angiogenesis. Furthermore, tumor growth in gal-1-null mice no longer responds to antiangiogenesis treatment by anginex. Thus, gal-1 regulates tumor angiogenesis and is a target for angiostatic cancer therapy.
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