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The transcription factor early growth response factor-1 (EGR-1) promotes apoptosis of neuroblastoma cells

AutorPignatelli, Miguel; Luna Medina, Rosario de ; Pérez-Rendón, Arturo; Santos, Ángel; Pérez Castillo, Ana
Palabras claveApoptosis
Cell death
Early genes
Fecha de publicación1-ago-2003
EditorPortland Press
CitaciónBiochemical Journal 373(P3): 739-746 (2003)
ResumenEarly growth response factor-1 (EGR-1) is an immediate early gene, which is rapidly activated in quiescent cells by mitogens or in postmitotic neurons after depolarization. EGR-1 has been involved in diverse biological functions such as cell growth, differentiation and apoptosis. Here we report that enforced expression of the EGR-1 gene induces apoptosis, as determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-fluorescein nick-end labelling (TUNEL) analysis, in murine Neuro2A cells. In accordance with this role of EGR-1 in cell death, antisense oligonucleotides increase cell viability in cells cultured in the absence of serum. This apoptotic activity of the EGR-1 appears to be mediated by p73, a member of the p53 family of proteins, since an increase in the amount of p73 is observed in clones stably expressing the EGR-1 protein. We also observed an increase in the transcriptional activity of the mdm2 promoter in cells overexpressing EGR-1, which is paralleled by a marked decrease in the levels of p53 protein, therefore excluding a role of this protein in mediating EGR-1-induced apoptosis. Our results suggest that EGR-1 is an important factor involved in neuronal apoptosis.
Descripción8 pages, 8 figures.
Versión del editorhttp://www.biochemj.org/bj/373/0739/bj3730739.htm
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