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

432 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)15975-15980
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume103
Issue number43
DOIs
StatePublished - Oct 24 2006

Keywords

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

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