The overexpression of Bcl-2 antagonizes the proapoptotic function of the kappa-opioid receptor

Ann N Y Acad Sci. 2003 Dec:1010:358-60. doi: 10.1196/annals.1299.066.

Abstract

Opioid receptors are G-protein-coupled cell-surface receptors that are mainly expressed in neuronal cells. Stimulation of the kappa-opioid receptor expressed by cultured human epithelial cancer cells promotes staurosporine-induced apoptosis. In this study, while Bcl-2 did not inhibit staurosporine-induced apoptosis, it did inhibit the kappa-opioid receptor-mediated potentiation of apoptosis. The results suggest that Bcl-2 targets a step that is specific to the signaling pathway of the kappa-opioid receptor.

MeSH terms

  • 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Cell Line, Tumor
  • Genes, bcl-2
  • Humans
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Receptors, Opioid, kappa / drug effects
  • Receptors, Opioid, kappa / physiology*
  • Staurosporine / pharmacology

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Opioid, kappa
  • 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
  • Staurosporine