Antiangiogenic effect of KR-31372 by apoptosis via mediation of mitochondrial KATP channel opening and the phosphatase and tensin homolog deleted from chromosome 10 phosphorylation

J Pharmacol Exp Ther. 2003 Jun;305(3):1142-9. doi: 10.1124/jpet.103.048819. Epub 2003 Mar 6.

Abstract

Antiangiogenic action of (2R,3R,4S)-N"-cyano-N-(6-nitro-3,4-dihydro-hydroxy-2-methyl-2-dimethoxymethyl-2H-1-benzopyran-4yl)-N'-benzyl guanidine (KR-31372) was examined with its proapoptotic action in human umbilical vein endothelial cells (HUVECs) compared with diazoxide. KR-31372 as well as diazoxide significantly suppressed the neovascularization in mice induced by the Matrigel-containing recombinant human vascular endothelial growth factor (VEGF)165 in vivo and the basal tube formation of HUVECs in vitro with suppression of proliferation of HUVECs stimulated by VEGF165. KR-31372 and diazoxide enhanced DNA fragmentation associated with increase in phosphatase and tensin homolog deleted from chromosome 10 (PTEN) and decrease in serine/threonine kinase phosphorylation, which were accompanied by augmented Bax and cytochrome c release, and suppressed Bcl-2 in HUVECs. In the U87-MG cells, when transfected with expression vectors for sense PTEN, KR-31372 enhanced DNA fragmentation, but not in naive U87-MG cells. The suppression by KR-31372 and diazoxide of these variables was significantly antagonized by 5-hydroxydecanoic acid, a mitochondrial KATP channel blocker. Taken together, KR-31372 strongly inhibited angiogenesis in HUVECs by proapoptotic mechanism via mediation of 5-hydroxydecanoic acid-inhibitable mitochondrial KATP channel opening and PTEN phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Apoptosis*
  • Benzopyrans / pharmacology*
  • Blotting, Western
  • Cell Division / drug effects
  • Cells, Cultured
  • Collagen
  • Cytochrome c Group / metabolism
  • Drug Combinations
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Humans
  • Laminin
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • PTEN Phosphohydrolase
  • Phosphoric Monoester Hydrolases / metabolism*
  • Phosphorylation
  • Potassium Channels
  • Protein Serine-Threonine Kinases*
  • Proteoglycans
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Tumor Suppressor Proteins / metabolism*
  • Umbilical Veins
  • bcl-2-Associated X Protein

Substances

  • Angiogenesis Inhibitors
  • BAX protein, human
  • Bax protein, mouse
  • Benzopyrans
  • Cytochrome c Group
  • Drug Combinations
  • KR 31372
  • Laminin
  • Membrane Proteins
  • Potassium Channels
  • Proteoglycans
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Proteins
  • bcl-2-Associated X Protein
  • mitochondrial K(ATP) channel
  • matrigel
  • Collagen
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Phosphoric Monoester Hydrolases
  • PTEN Phosphohydrolase
  • PTEN protein, human