Document Detail

Deregulated expression of the retinoid X receptor alpha prevents muscle differentiation in P19 embryonal carcinoma cells.
MedLine Citation:
PMID:  9751115     Owner:  NLM     Status:  MEDLINE    
We have studied the expression of the retinoid X receptor (RXR) family of receptors during the DMSO-induced differentiation of P19 murine embryonal carcinoma cells into mesoderm and muscle. RXR-alpha protein is weakly detectable in untreated P19 cells and in a mutant line of P19 cells (D3) that are resistant to DMSO-induced differentiation but begins to increase by day 3 and continues to rise gradually thereafter, whereas RXR-gamma protein is readily detected in P19 cells and decreases over the course of differentiation. Protein expression is uncoupled from mRNA levels, because DMSO induces a rapid, aggregation-independent, transient increase in RXR-alpha mRNA that diminishes by day 3 of differentiation. Thus, the expression of RXR-alpha protein is prevented at early times during DMSO-induced differentiation. Stable P19 cell clones that constitutively express RXR-alpha protein [P19(RXR-alpha)] are resistant to DMSO-induced differentiation associated with increased levels of oligonucleosomal-length DNA fragmentation. Loss of RXR-alpha expression after multiple passages results in a reversion to a DMSO-responsive phenotype. Id1 transcripts are present in P19 cells and are transiently decreased on day 2 of DMSO differentiation but remain elevated in DMSO-treated P19(RXR-alpha) and in P19 cells treated simultaneously with retinoic acid and DMSO. The mRNA for the mesoderm inducer protein Brachyury T was also deregulated in P19(RXR-alpha) cells and D3 cells compared with that of wild-type P19 cells. Together, these results show that expression of the RXR-alpha mRNA and protein in P19 cells is tightly regulated during the mesodermal/muscle differentiation of P19 cells, and that ectopic expression of the RXR-alpha protein prevents differentiation associated with increased cell death, prolonged expression of Brachyury T, and constitutive expression of Id1.
M A Pratt; C Crippen; K Hubbard; M Menard
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research     Volume:  9     ISSN:  1044-9523     ISO Abbreviation:  Cell Growth Differ.     Publication Date:  1998 Sep 
Date Detail:
Created Date:  1998-12-11     Completed Date:  1998-12-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9100024     Medline TA:  Cell Growth Differ     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  713-22     Citation Subset:  IM    
Department of Pharmacology, University of Ottawa, Ontario, Canada.
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MeSH Terms
Administration, Topical
Anti-Inflammatory Agents / pharmacology
Carcinoma, Embryonal / genetics*,  pathology
Cell Death / drug effects
Cell Differentiation / drug effects,  genetics
Clone Cells / cytology,  metabolism
Dimethyl Sulfoxide / pharmacology
Gene Expression Regulation, Neoplastic
Muscles / cytology*,  drug effects,  metabolism
Receptors, Retinoic Acid / drug effects,  genetics*,  metabolism
Retinoid X Receptors
Transcription Factors / drug effects,  genetics*,  metabolism
Tumor Cells, Cultured
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Receptors, Retinoic Acid; 0/Retinoid X Receptors; 0/Transcription Factors; 67-68-5/Dimethyl Sulfoxide

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