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Suradista NSC 651016 inhibits the angiogenic activity of CXCL12-stromal cell-derived factor 1 alpha

  1. Author:
    Schneider, G. P.
    Salcedo, R.
    Dong, H. F.
    Kleinman, H. K.
    Oppenheim, J. J.
    Howard, O. M. Z.

  2. Author Address

    NCI, POB B, Frederick, MD 21702 USA NCI, Frederick, MD 21702 USA Sci Applicat Int Corp, Mol Immunoregulat Lab, Frederick, MD USA Sci Applicat Int Corp, Canc Res Ctr, Intramural Res Support Program, Frederick, MD USA Natl Inst Dent & Craniofacial Res, Cell Biol Sect, Bethesda, MD 20892 USA Howard OMZ NCI, POB B, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Clinical Cancer Research
    1. 8
    2. 12
    3. Pages: 3955-3960
  4. Type of Article: Article
  1. Abstract:

    CXCL12 (stromal cell-derived factor let), a ligand for CXCR4, has been shown to induce endothelial cell chemotaxis and to stimulate angiogenesis, suggesting that it may be a significant target for antiangiogenic therapy. Here we have tested suradista NSC 651016, a compound known to inhibit CXCL12- induced monocyte chemotaxis, for its ability to inhibit CXCL12- induced angiogenic activity. NSC 651016 inhibited CXCL12- mediated endothelial cell chemotaxis in a dose-dependent manner. In addition, new vessel sprouting, by both rat and chick aorta in an angiogenesis model, was inhibited. Additionally, in vitro capillary-like structure formation induced by CXCL12 was inhibited by NSC 651016. Furthermore, NSC 651016 inhibited CXCL12-mediated angiogenesis in an in vivo s.c. assay. These data indicate that suradista NSC 651016 possesses in vitro and in vivo antiangiogenic activity and has the potential to interfere with neovacularization of tumors and their metastases.

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