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C/EBP α and β mimic retinoic acid activation of IGFBP-5 in neuroblastoma cells by a mechanism independent from binding to their site

TitoloC/EBP α and β mimic retinoic acid activation of IGFBP-5 in neuroblastoma cells by a mechanism independent from binding to their site
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2005
AutoriCesi, Vincenzo, Giuffrida M.L., Vitali Roberta, Tanno Barbara, Mancini C., Calabretta B., and Raschellà Giuseppe
RivistaExperimental Cell Research
Volume305
Paginazione179-189
ISSN00144827
Parole chiaveanalytic method, animal cell, article, binding site, CCAAT enhancer binding protein alpha, CCAAT enhancer binding protein beta, cell differentiation, chromatin, comparative study, controlled study, human, human cell, Immunoprecipitation, mutation, neuroblastoma cell, nonhuman, nucleotide, nucleotide sequence, priority journal, promoter region, protein binding, protein expression, protein function, Retinoic acid, somatomedin binding protein 5, TATA box, transcription factor, transcription initiation
Abstract

Signal transduction mediated by insulin-like growth factors is implicated in the aggressive behavior of neuroblastoma (NB), a childhood tumor originating from the neural crest. IGFBP-5, a protein that binds IGFs with high affinity, is expressed in many NB cell lines exerting opposite effects, depending on its concentration. We found that IGFBP-5 expression increased during retinoic acid (RA)-mediated differentiation of NB cells. This was due to transcriptional activation as demonstrated by reporter assays carried out in basal and differentiating conditions. We defined the shortest region of the human IGFBP-5 promoter (from nucleotide -83 to +53) which is sensitive to RA. Mutation of a CCAAT enhancer binding protein (C/EBP) element inside this region increased transcription, suggesting a repressive role of this sequence. DNA Affinity Precipitation Assays (DAPA) and chromatin immunoprecipitation demonstrated that the binding of C/EBPα and β to the C/EBP site decreased upon treatment with RA. C/EBPα and β induced an increase in IGFBP-5 transcription in human and murine NB cells similar to that obtained upon RA treatment. Activation by C/EBP α and β did not depend on their binding to the C/EBP site, since they still activated IGFBP-5 promoter carrying a mutation in the C/EBP site. Of interest, we found that both transcription factors were able to interact with the TATA box, but only C/EBPα interaction increased during RA-induced differentiation. © 2005 Elsevier Inc. All rights reserved.

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cited By 11

URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-15044360253&doi=10.1016%2fj.yexcr.2004.12.015&partnerID=40&md5=4652a3382921b3dc9c45b05d16c8fd6f
DOI10.1016/j.yexcr.2004.12.015
Citation KeyCesi2005179