Document Detail

Induction of Id-1 by FGF-2 involves activity of EGR-1 and sensitizes neuroblastoma cells to cell death.
MedLine Citation:
PMID:  21506108     Owner:  NLM     Status:  MEDLINE    
Inhibitor of differentiation-1 (Id-1) is a member of helix-loop-helix (HLH) family of proteins that regulate gene transcription through their inhibitory binding to basic-HLH transcription factors. Similarly to other members of this family, Id-1 is involved in the repression of cell differentiation and activation of cell growth. The dual function of Id-1, inhibition of differentiation, and stimulation of cell proliferation, might be interdependent, as cell differentiation is generally coupled with the exit from the cell cycle. Fibroblast growth factor-2 (FGF-2) has been reported to play multiple roles in different biological processes during development of the central nervous system (CNS). In addition, FGF-2 has been described to induce "neuronal-like" differentiation and trigger apoptosis in neuroblastoma SK-N-MC cells. Although regulation of Id-1 protein by several mitogenic factors is well-established, little is known about the role of FGF-2 in the regulation of Id-1. Using human neuroblastoma cell line, SK-N-MC, we found that treatment of these cells with FGF-2 resulted in early induction of both Id-1 mRNA and protein. The induction occurs within 1 h from FGF-2 treatment and is mediated by ERK1/2 pathway, which in turn stimulates expression of the early growth response-1 (Egr-1) transcription factor. We also demonstrate direct interaction of Egr-1 with Id-1 promoter in vitro and in cell culture. Finally, inhibition of Id-1 expression results in G(2) /M accumulation of FGF-2-treated cells and delayed cell death.
Giovanni Passiatore; Antonio Gentilella; Slava Rom; Marco Pacifici; Valeria Bergonzini; Francesca Peruzzi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  226     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-04-20     Completed Date:  2011-06-17     Revised Date:  2013-09-09    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1763-70     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Wiley-Liss, Inc.
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA.
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MeSH Terms
Binding Sites
Brain Neoplasms / genetics,  metabolism*,  pathology
Cell Cycle
Cell Line, Tumor
Early Growth Response Protein 1 / metabolism*
Fibroblast Growth Factor 2 / metabolism*
Gene Expression Regulation, Neoplastic
Inhibitor of Differentiation Protein 1 / genetics,  metabolism*
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Neuroblastoma / genetics,  metabolism*,  pathology
Promoter Regions, Genetic
RNA Interference
RNA, Messenger / metabolism
Recombinant Proteins / metabolism
Time Factors
Grant Support
Reg. No./Substance:
0/EGR1 protein, human; 0/Early Growth Response Protein 1; 0/ID1 protein, human; 0/Inhibitor of Differentiation Protein 1; 0/RNA, Messenger; 0/Recombinant Proteins; 103107-01-3/Fibroblast Growth Factor 2; EC protein, human; EC Protein Kinase 1; EC Protein Kinase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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