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Halofuginone: A potent inhibitor of critical steps in angiogenesis progression
Year:
2000
Source of publication :
FASEB Journal
Authors :
Pines, Mark
;
.
Volume :
14
Co-Authors:
Elkin, M., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Miao, H.-Q., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Nagler, A., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Aingorn, E., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Reich, R., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Hemo, I., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Dou, H.-L., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Pines, M., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Vlodavsky, I., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Facilitators :
From page:
2477
To page:
2485
(
Total pages:
9
)
Abstract:
We have previously demonstrated that halofuginone, a low molecular weight quinazolinone alkaloid, is a potent inhibitor of collagen cd (I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also effectively suppresses tumor progression and metastasis in mice. These results together with the well-documented role of extracellular matrix (ECM) components and matrix degrading enzymes in formation of new blood vessels led us to investigate the effect of halofuginone on the anglogenic process. In a variety of experimental system, representing sequential events in the angiogenic cascade, halofuginone treatment resulted in profound inhibitory effect. Among these are the abrogation of endothelial cell MMP-2 expression and basement membrane invasion, capillary tube formation, and vascular sprouting, as well as deposition of subendothelial ECM. The most conclusive anti-angiogenic activity of halofuginone was demonstrated in vivo (mouse corneal micropocket assay) by showing a marked inhibition of basic fibroblast growth factor (bFGF) -induced neovascularization in response to systemic administration of halofuginone, either i.p. or in the diet. The ability of halofuginone to interfere with key events in neovascularization, together with its oral bioavailability and safe use as an anti-parasitic agent, make it a promising drug for further evaluation in the treatment of a wide range of diseases associated with pathological angiogenesis.
Note:
Related Files :
Animals
animal tissue
Capillaries
cattle
drug effect
Drug Safety
endothelium cell
neovascularization (pathology)
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More details
DOI :
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
32347
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:09
Scientific Publication
Halofuginone: A potent inhibitor of critical steps in angiogenesis progression
14
Elkin, M., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Miao, H.-Q., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Nagler, A., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Aingorn, E., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Reich, R., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Hemo, I., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Dou, H.-L., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Pines, M., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Vlodavsky, I., Department of Oncology, Hadassah Hospital, POB 12000, Jerusalem 91120, Israel
Halofuginone: A potent inhibitor of critical steps in angiogenesis progression
We have previously demonstrated that halofuginone, a low molecular weight quinazolinone alkaloid, is a potent inhibitor of collagen cd (I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also effectively suppresses tumor progression and metastasis in mice. These results together with the well-documented role of extracellular matrix (ECM) components and matrix degrading enzymes in formation of new blood vessels led us to investigate the effect of halofuginone on the anglogenic process. In a variety of experimental system, representing sequential events in the angiogenic cascade, halofuginone treatment resulted in profound inhibitory effect. Among these are the abrogation of endothelial cell MMP-2 expression and basement membrane invasion, capillary tube formation, and vascular sprouting, as well as deposition of subendothelial ECM. The most conclusive anti-angiogenic activity of halofuginone was demonstrated in vivo (mouse corneal micropocket assay) by showing a marked inhibition of basic fibroblast growth factor (bFGF) -induced neovascularization in response to systemic administration of halofuginone, either i.p. or in the diet. The ability of halofuginone to interfere with key events in neovascularization, together with its oral bioavailability and safe use as an anti-parasitic agent, make it a promising drug for further evaluation in the treatment of a wide range of diseases associated with pathological angiogenesis.
Scientific Publication
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