Galectin-1 is essential in tumor angiogenesis and is a target for antiangiogenesis therapy

Victor L.J.L. Thijssen, Ruben Postel, Ricardo J.M.G.E. Brandwijk, Ruud P.M. Dings, Irina Nesmelova, Sietske Satijn, Nicole Verhofstad, Yusaku Nakabeppu, Linda G. Baum, Jeroen Bakkers, Kevin H. Mayo, Françoise Poirier, Arjan W. Griffioen

Research output: Contribution to journalArticlepeer-review

406 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)15975-15980
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number43
StatePublished - Oct 24 2006


  • Anginex
  • Angiostatic therapy
  • Endothelial cell
  • Galectin
  • Tumor models


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