Document Detail

Regulation of transcription of the intracellular interleukin-1 receptor antagonist gene by AP-1 in mouse carcinoma cells.
MedLine Citation:
PMID:  11933077     Owner:  NLM     Status:  MEDLINE    
Interleukin-1 receptor antagonist (IL-1Ra) is involved in many processes, including epidermal inflammation and hyperplasia after irritation or injury. However, the mechanism by which intracellular IL-1Ra (icIL-1Ra) expression is regulated in mouse keratinocytes has not been reported. We found that the CH72 mouse carcinoma cell line constitutively expresses the icIL-1Ra mRNA. To study the transcriptional factors responsible for the constitutive expression of icIL-1Ra, we functionally characterized 4.5 kb of the 5' flanking region of the human icIL-1Ra gene in these cells. We first demonstrated that icIL-1Ra expression in these cells was regulated at the level of transcription. Deletion analysis of the promoter showed that regulatory elements for constitutive expression were located -158 to -49 bp upstream of the transcription start site for icIL-1Ra. We investigated the cis- and trans-acting factors required for icIL-1Ra expression. An activating protein-1 (AP-1) site was identified as the positive regulatory element necessary for the constitutive expression of the icIL-1Ra promoter in CH72 cells. Moreover, electrophoretic mobility shift assay and cotransfection experiments showed that c-jun and c-fos proteins bound to the AP-1 site and functionally transactivated the icIL-1Ra promoter in mouse carcinoma CH72 cells.
Eunhye La; Joyce E Rundhaug; Amy Pavone; Susan M Fischer
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular carcinogenesis     Volume:  33     ISSN:  0899-1987     ISO Abbreviation:  Mol. Carcinog.     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-04-04     Completed Date:  2002-05-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8811105     Medline TA:  Mol Carcinog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  237-43     Citation Subset:  IM    
Copyright Information:
Copyright 2002 Wiley-Liss, Inc.
The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, Texas 78957, USA.
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MeSH Terms
Base Sequence
Carcinoma, Squamous Cell
Consensus Sequence
Gene Expression Regulation, Neoplastic / physiology*
Genes, Reporter
Interleukin 1 Receptor Antagonist Protein
Luciferases / genetics,  metabolism
Recombinant Proteins / metabolism
Sequence Alignment
Sequence Deletion
Sialoglycoproteins / genetics*
Skin Neoplasms
Transcription Factor AP-1 / metabolism*
Transcription, Genetic / physiology*
Tumor Cells, Cultured
Grant Support
Reg. No./Substance:
0/IL1RN protein, human; 0/Il1rn protein, mouse; 0/Interleukin 1 Receptor Antagonist Protein; 0/Recombinant Proteins; 0/Sialoglycoproteins; 0/Transcription Factor AP-1; EC 1.13.12.-/Luciferases

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