A novel mechanism of resistance to α-difluoromethylornithine induced by cycloheximide. Growth with abnormally low levels of putrescine and spermidine

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Treatment of the chemically transformed fibroblasts BP-A31 and other cell lines with low concentrations of cycloheximide (CHM) for 72 h followed by the removal of the protein synthesis inhibitor leads to the proliferation of α-difluoromethylornithine (DFMO)-resistant phenotypes. These drug-resistant...

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Detalles Bibliográficos
Autores principales: Medrano, E.E., Burrone, O.R., Ferrer, M.M., Cafferata, E.G.A., Algranati, I.D.
Formato: Artículo publishedVersion
Lenguaje:Inglés
Publicado: 1986
Materias:
Cycloheximide
Ornithine decarboxylase
Polyamine
α-Difluoromethylornithine resistance
cycloheximide
eflornithine
putrescine
spermidine
cell line
drug inhibition
drug resistance
fibroblast
in vitro study
nonhuman
priority journal
Animals
Cell Line
Drug Resistance
Eflornithine
Fibroblasts
Humans
Mice
Ornithine Decarboxylase
Putrescine
Spermidine
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00145793_v206_n1_p106_Medrano
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:Treatment of the chemically transformed fibroblasts BP-A31 and other cell lines with low concentrations of cycloheximide (CHM) for 72 h followed by the removal of the protein synthesis inhibitor leads to the proliferation of α-difluoromethylornithine (DFMO)-resistant phenotypes. These drug-resistant cells contain almost no ornithine decarboxylase (ODC) activity and concomitantly very low levels of putrescine and spermidine. Southern blot analysis and measurements of ODC activity and intracellular polyamine levels showed that the described mechanism of inducing resistance to DFMO triggered by CHM does not involve ODC gene amplification, altered transport of the drug or reduced affinity of the enzyme for DFMO. © 1986.

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