Apoptosis induced by protein kinase C inhibition in a neuroblastoma cell line

Cell Growth Differ. 1995 Nov;6(11):1375-80.

Abstract

The protein kinase C inhibitor bisindolylmaleimide GF109203X has a dual effect on the behavior of the neuroblastoma cell line Neuro-2A; when the inhibitor is added in conditions that induce differentiation (absence of serum), neurite outgrowth is potentiated in a dose-dependent manner. However, if the inhibitor is added in growth-promoting conditions (presence of serum), programmed cell death (apoptosis) is induced, as assessed by internucleosomal DNA cleavage and specific immunoassays. This effect is also seen with other specific protein kinase C inhibitors. Bcl2 gene overexpression protects Neuro-2A cells from apoptosis, as has been found in other systems. We also show that calpain I, a neutral Ca(2+)-activated proteinase, participates in this apoptotic pathway. Our results point to a key role of protein kinase C in the regulation of growth and differentiation in Neuro-2A cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Blood Proteins / pharmacology
  • Calpain / pharmacology
  • Cell Differentiation / physiology
  • Cell Division / drug effects
  • Enzyme Inhibitors / pharmacology*
  • Gene Expression / physiology
  • Indoles / pharmacology*
  • Maleimides / pharmacology*
  • Mice
  • Neuroblastoma*
  • Protein Kinase C / antagonists & inhibitors*
  • Protein-Tyrosine Kinases / genetics
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Cells, Cultured / cytology

Substances

  • Blood Proteins
  • Enzyme Inhibitors
  • Indoles
  • Maleimides
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Protein-Tyrosine Kinases
  • Protein Kinase C
  • Calpain
  • bisindolylmaleimide I