Glucocorticoid-mediated inhibition of ornithine decarboxylyase activity in S49 lymphoma cells.
AUTOR(ES)
Insel, P A
RESUMO
Incubation of wild-type S49 lymphoma cells with glucocorticoids, such as dexamethasone and hydrocortisone, inhibits the activity of ornithine decarboxylase (L-ornithine carboxylyase, EC 4.1.1.17), the rate-limiting enzyme in the pathway of polyamine biosynthesis. The kinetics of this inhibition are more rapid than the glucocorticoid-mediated growth arrest in the G1 phase of the cell cycle or in glucocorticoid-mediated cytolysis of these cells. The inhibition of ornithine decarboxylase activity by corticosteroids is specific for steroids of the glucocorticoid class. Results obtained with variant S49 cells having lesions in the pathways of glucocorticoid or cyclic AMP action indicate that cytoplasmic glucocorticoid receptors, as well as nuclear transfer of steroid--receptor complexes, are required for the inhibition of ornithine decarboxylase activity but that this inhibition does not require hormonal activation of adenylate cyclase or cyclic AMP-dependent protein kinase. Because glucocorticoid-mediated inhibition of ornithine decarboxylase occurs when cellular protein synthesis has decreased less than 20%, this inhibition may represent a specific glucocorticoid-mediated deinduction of ornithine decarboxylase in S49 cells. Inhibition of ornithine decarboxylase activity may offer a useful marker for suppression of growth and cell cycle progression in these and other lymphoma cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=348823Documentos Relacionados
- Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.
- Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras.
- Protein kinase A activation of glucocorticoid-mediated signaling in the developing retina.
- Adenylate cyclase permanently uncoupled from hormone receptors in a novel variant of S49 mouse lymphoma cells.
- Residual nitrobenzylthioinosine-resistant nucleoside transport in a transport mutant (AE1) of S49 murine T-lymphoma cells.
