PUBLICATION

Phostine 3.1a as a pharmacological compound with antiangiogenic properties against diseases with excess vascularization

Authors
Bousseau, S., Marchand, M., Soleti, R., Vergori, L., Hilairet, G., Recoquillon, S., Le Mao, M., Gueguen, N., Khiati, S., Clarion, L., Bakalara, N., Martinez, M.C., Germain, S., Lenaers, G., Andriantsitohaina, R.
ID
ZDB-PUB-190301-8
Date
2019
Source
FASEB journal : official publication of the Federation of American Societies for Experimental Biology   33(5): 5864-5875 (Journal)
Registered Authors
Keywords
angiogenesis, cancer growth, endothelial metabolism, glycosylation, pharmacotherapy
MeSH Terms
  • Cell Line, Tumor
  • Glioblastoma/metabolism
  • Cell Proliferation
  • Adenosine Triphosphate/metabolism
  • Vascular Endothelial Growth Factor A/metabolism
  • Extracellular Matrix/metabolism
  • Phosphines/pharmacology*
  • Cell Movement/drug effects
  • Animals
  • Adenosine Diphosphate/metabolism
  • Male
  • Angiogenesis Inhibitors/pharmacology*
  • Endothelial Cells/metabolism
  • Galectin 1/metabolism
  • Zebrafish
  • Neovascularization, Pathologic/drug therapy*
  • Neoplasm Transplantation
  • Signal Transduction/drug effects
  • Apoptosis
  • Vascular Endothelial Growth Factor Receptor-2/metabolism
  • Glycosylation
  • Mice
  • Humans
  • Mice, Nude
  • Cell Adhesion
  • Human Umbilical Vein Endothelial Cells
PubMed
30817178 Full text @ FASEB J.
Abstract
Angiogenesis is a complex process leading to the growth of new blood vessels from existing vasculature, triggered by local proangiogenic factors such as VEGF. An excess of angiogenesis is a recurrent feature of various pathologic conditions such as tumor growth. Phostines are a family of synthetic glycomimetic compounds that exhibit anticancer properties, and the lead compound 3-hydroxy-4,5-bis-benzyloxy-6-benzyloxymethyl-2-phenyl2-oxo-2λ5-[1,2]oxaphosphinane (PST 3.1a) shows antiglioblastoma properties both in vitro and in vivo. In the present study, we assessed the effect of PST 3.1a on angiogenesis and endothelial metabolism. In vitro, PST 3.1a (10 µM) inhibited all steps that regulate angiogenesis, including migration, proliferation, adhesion, and tube formation. In vivo, PST 3.1a reduced intersegmental vessel formation and vascularization of the subintestinal plexus in zebrafish embryos and also altered pathologic angiogenesis and glioblastoma progression in vivo. Mechanistically, PST 3.1a altered interaction of VEGF receptor 2 and glycosylation-regulating protein galectin-1, a key component regulating angiogenesis associated with tumor resistance. Thus, these data show that use of PST 3.1a is an innovative approach to target angiogenesis.-Bousseau, S., Marchand, M., Soleti, R., Vergori, L., Hilairet, G., Recoquillon, S., Le Mao, M., Gueguen, N., Khiati, S., Clarion, L., Bakalara, N., Martinez, M. C., Germain, S., Lenaers, G., Andriantsitohaina, R. Phostine 3.1a as a pharmacological compound with antiangiogenic properties against diseases with excess vascularization.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping