Skip NavigationSkip to Content
Return Return to Search Results

The anti-cancer compound Nordy inhibits CXCR4-mediated production of IL-8 and VEGF by malignant human glioma cells

  1. Author:
    Ping, Y. F.
    Yao, X. H.
    Chen, J. H.
    Liu, H.
    Chen, D. L.
    Zhou, X. D.
    Wang, J. M.
    Bian, X. W.

  2. Author Address

    Third Mil Med Univ, SW Hosp, Inst Pathol, Chongqing 400038, Peoples R China. Third Mil Med Univ, Div Basic Med Sci, Dept Pharm, Chongqing 400038, Peoples R China. NCI, Ctr Canc Res, Mol Immunoregulat Lab, Frederick, MD 21702 USA.;Bian, XW, Third Mil Med Univ, SW Hosp, Inst Pathol, Chongqing 400038, Peoples R China.;bianxiuwu@263.net
    1. Year: 2007
    2. Date: Aug
  2. Journal: Journal of Neuro-Oncology
    1. 84
    2. 1
    3. Pages: 21-29
  4. Type of Article: Article
  5. ISSN: 0167-594X
  1. Abstract:

    The chemokine receptor CXCR4 plays an important role in tumor growth, angiogenesis and metastasis. Our previous studies showed that Nordy, a synthetic chiral compound of nordihydroguaiaretic acid, inhibited the growth and angiogenesis of various malignant tumors. In this study we examined the capacity of Nordy to regulate CXCR4-mediated production of angiogenic factors by human glioblastoma cells. We found that Nordy potently inhibited CXCR4 ligand SDF-1-induced production of IL-8 and vascular endothelial cell growth factor, two important angiogenic factors implicated in the progression of malignant tumors. Further study revealed that the effect of Nordy was attributable to its down-regulation of the expression of functional CXCR4 in glioblastoma cells. These results suggest that the anti-cancer activity of Nordy is due, at least in part, to its suppression of the chemokine receptor CXCR4 thus reducing the production of angiogenic factors by tumor cells.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1007/s11060-007-9349-8
  3. View record in Web of Science®
  4. WOS: 000248006700003

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel