Document Detail


Overexpression of E2F1 in glioma-derived cell lines induces a p53-independent apoptosis that is further enhanced by ionizing radiation.
MedLine Citation:
PMID:  11302249     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glioma cell lines show variable responses to radiation in a manner influenced by their p53 status. Irradiation of glioma cell lines does not generally induce apoptosis. When wild-type p53 is present, these cells undergo a G1 arrest that is closely associated with increased radiosensitivity as measured by clonogenic survival. Previously, others have shown that dysregulated overexpression of E2F1 induces apoptosis in cell lines with either functional or inactivated p53. We found that regardless of p53 status, apoptosis induced by overexpression of E2F1 in glioma cell lines was further enhanced by treatment with ionizing radiation. BAX induction did not follow E2F1 overexpression or irradiation in the glioma cell lines tested. Thus, the apoptotic response of glioma-derived cells to irradiation can be enhanced by E2F1 by a mechanism that does not involve the induction of BAX.
Authors:
H K Shu; C M Julin; F Furman; G L Yount; D Haas-Kogan; M A Israel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neuro-oncology     Volume:  2     ISSN:  1522-8517     ISO Abbreviation:  Neuro-oncology     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2001-04-13     Completed Date:  2001-05-03     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100887420     Medline TA:  Neuro Oncol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  16-21     Citation Subset:  IM    
Affiliation:
Department of Neurological Surgery, University of California, San Francisco 94143, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / physiology*
Carrier Proteins*
Caspases / metabolism
Cell Cycle Proteins*
DNA-Binding Proteins*
E2F Transcription Factors
E2F1 Transcription Factor
Enzyme Activation / physiology
Glioma / metabolism*,  pathology
Proto-Oncogene Proteins / physiology
Proto-Oncogene Proteins c-bcl-2*
Radiation, Ionizing*
Retinoblastoma-Binding Protein 1
Transcription Factors / metabolism*
Transcriptional Activation / physiology
Tumor Cells, Cultured / metabolism,  radiation effects
Tumor Suppressor Protein p53 / physiology*
bcl-2-Associated X Protein
Grant Support
ID/Acronym/Agency:
CA 09215/CA/NCI NIH HHS; CA 13525/CA/NCI NIH HHS; CA 64898/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/E2F Transcription Factors; 0/E2F1 Transcription Factor; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Retinoblastoma-Binding Protein 1; 0/Transcription Factors; 0/Tumor Suppressor Protein p53; 0/bcl-2-Associated X Protein; EC 3.4.22.-/Caspases

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


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