Apoptosis induced by N-hexanoylsphingosine in CHP-100 cells associates with accumulation of endogenous ceramide and is potentiated by inhibition of glucocerebroside synthesis

Cell Death Differ. 1998 Sep;5(9):785-91. doi: 10.1038/sj.cdd.4400428.

Abstract

We report that apoptosis induced by N-hexanoylsphingosine (C6-Cer) in CHP-100 human neuroepithelioma cells associates with accumulation of monohexosylsphingolipids produced not only by short-chain ceramide glycosylation but also through glycosylation of a ceramide pool endogenously produced. By high-performance thin layer chromatography on borate silica gel plates, newly formed monohexosylsphingolipids were identified as glucosylceramides (GluCer); however, accumulation of lactosylceramide or higher-order glycosphingolipids was not observed. GluCer accumulation was fully suppressed by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol; moreover, while this inhibitor had no effect on cell viability when administered alone, it markedly potentiated the apoptotic effect of C6-Cer. These results provide evidence that activation of GluCer synthesis is an important mechanism through which CHP-100 cells attempt to escape ceramide-induced apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Ceramides / metabolism*
  • Ceramides / pharmacology
  • Glucosylceramides / biosynthesis*
  • Glucosylceramides / metabolism*
  • Glycosphingolipids / metabolism
  • Glycosylation
  • Humans
  • Tumor Cells, Cultured

Substances

  • Ceramides
  • Glucosylceramides
  • Glycosphingolipids
  • N-caproylsphingosine