Document Detail


Transcriptional repression of the eukaryotic initiation factor 4E gene by wild type p53.
MedLine Citation:
PMID:  16112647     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The eukaryotic initiation factor 4E (eIF4E) plays important roles in transformation and cancer progression. It is frequently overexpressed in malignant cells, one mechanism of which is through transcriptional activation by c-myc. Here, we report that high level of eIF4E expression and its tumorigenicity could be alternatively associated with defects of p53, since we found that induction of wt-p53 repressed eIF4E expression. Gene transfection of p53 inhibited eIF4E promoter activity, while inactivation of p53 either by mutation or by over-expression of MDM2 resulted in stimulation of eIF4E promoter activity. We demonstrated that p53-repression of eIF4E was regulated by c-myc. The wt-p53 can physically bind to c-myc, which inhibited binding of c-myc to eIF4E promoter and c-myc-stimulated promoter activity. These results suggest that the expression of eIF4E is reciprocally regulated by p53 and c-myc, and loss of p53-mediated control over c-myc-dependent transactivation of eIF4E may represent a novel mechanism for eIF4E-mediated neoplastic transformation and cancer progression.
Authors:
Ningxi Zhu; Lubing Gu; Harry W Findley; Muxiang Zhou
Related Documents :
1577267 - A targeted mutation reveals a role for n-myc in branching morphogenesis in the embryoni...
3855567 - Comparison of chemically induced and spontaneous murine thymic lymphomas in rf and akr ...
15522957 - Deregulated expression of the myc cellular oncogene drives development of mouse "burkit...
3211147 - The human fgf-5 oncogene encodes a novel protein related to fibroblast growth factors.
16352457 - Green tea polyphenol inhibits mycobacterium tuberculosis survival within human macropha...
18943887 - Four near-isogenic lines of cotton with different genes for bacterial blight resistance.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  335     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-08-30     Completed Date:  2005-11-14     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1272-9     Citation Subset:  IM    
Affiliation:
Division of Pediatric Hematology/Oncology/BMT, Emory University School of Medicine, Atlanta, GA, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Cell Line, Tumor
Child
Eukaryotic Initiation Factor-4E / metabolism*
Humans
Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
Transcription Factors / metabolism*
Transcriptional Activation*
Tumor Suppressor Protein p53 / metabolism*
Grant Support
ID/Acronym/Agency:
R01 CA82323/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Eukaryotic Initiation Factor-4E; 0/Transcription Factors; 0/Tumor Suppressor Protein p53

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


Previous Document:  Humoral detection of leukaemia-associated antigens in presentation acute myeloid leukaemia.
Next Document:  Ascorbic acid promotes osteoclastogenesis from embryonic stem cells.