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 language | English |
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Pages (from-to) | 15975-80 |
Number of pages | 6 |
Journal | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA |
Volume | 103 |
Issue number | 43 |
DOIs | |
Publication status | Published - 24 Oct 2006 |
Externally published | Yes |
Keywords
- Animals
- Cell Movement
- Cell Proliferation
- Cells, Cultured
- Disease Progression
- Endothelial Cells/metabolism
- Galectin 1/deficiency
- Gene Expression Regulation, Neoplastic
- Humans
- Mice
- Mice, Knockout
- Neoplasm Transplantation
- Neoplasms/blood supply
- Protein Binding
- Proteins/metabolism
- Zebrafish