The overexpression of Bcl-2 antagonizes the proapoptotic function of the kappa-opioid receptor.
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.
Wong
Naisum
N
Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Hong Kong. nswong@hkucc.hku.hk
Diao
Catherine Teimei
CT
Wong
Takming
T
D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D045744:Cell Line, Tumor; D019254:Genes, bcl-2; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics*; D017473:Receptors, Opioid, kappa / Q000187:drug effects / Q000502:physiology*; D019311:Staurosporine / Q000494:pharmacology
D019253:Proto-Oncogene Proteins c-bcl-2; D017473:Receptors, Opioid, kappa; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D019311:Staurosporine