Lipoxygenase inhibitors block CD95 ligand-mediated apoptosis of human malignant glioma cells

FEBS Lett. 1997 Jun 2;409(1):17-23. doi: 10.1016/s0014-5793(97)00468-7.

Abstract

CD95 ligand is a cytotoxic cytokine that induces apoptosis. Here we report that CD95-mediated apoptosis of human malignant glioma cells is associated with arachidonic acid (AA) release. Inhibitors of phospholipase A2, phospholipase C or diacylglycerol lipase have minor effects on AA release and fail to modulate apoptosis. Formation of two AA metabolites generated during CD95-dependent apoptosis is attenuated by the lipoxygenase inhibitor, nordihydroguaretic acid (NDGA). NDGA also blocks CD95 ligand-induced apoptosis. This effect is independent of antioxidant properties of NDGA. Lipoxygenase may thus play a critical role in CD95 ligand-induced apoptosis of human malignant glioma cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / immunology*
  • Arachidonic Acid / metabolism
  • Fas Ligand Protein
  • Glioma / immunology
  • Glioma / metabolism
  • Glioma / therapy*
  • Humans
  • Ligands
  • Lipoxygenase Inhibitors / pharmacology*
  • Masoprocol / pharmacology
  • Membrane Glycoproteins / physiology*
  • Mice
  • Phospholipases / antagonists & inhibitors
  • Tumor Cells, Cultured
  • fas Receptor / metabolism*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Ligands
  • Lipoxygenase Inhibitors
  • Membrane Glycoproteins
  • fas Receptor
  • Arachidonic Acid
  • Masoprocol
  • Phospholipases