Document Detail

Interleukin-3 dependent mitogenesis in murine cells involves a predominant non-protein kinase C (pKC) dependent pathway for c-myc transcription. Role of a myc expression vector in rescuing pKC dependent mitogenesis.
MedLine Citation:
PMID:  1774959     Owner:  NLM     Status:  MEDLINE    
The signaling pathways used by interleukin-3 (IL-3) and by active phorbol ester (12-0-tetradecanoyl phorbol-13-acetate, TPA) to stimulate mitogenesis in the growth factor dependent myeloid cell line FDC-P1 were studied by 'reporter' analysis of nuclear proto-oncogene expression. These studies revealed that IL-3 strongly stimulated c-myc expression by a transcriptional mechanism but IL-3 poorly stimulated c-jun expression, a measure of protein kinase C dependent signals. On the other hand, the protein kinase C agonist, TPA, strongly activated c-jun expression but poorly promoted expression (transcription) of c-myc in FDC-P1. These findings appeared to correlate with the poor mitogenic capacity of TPA for FDC-P1. However, stable transfection of FDC-P1 with a c-myc expression vector driven by a human methallothionein IIA promoter containing the TPA responsive element (TRE), led to a cell clone, FDMT myc.A1, in which TPA mediated selective transcription of the transfected TRE driven c-myc vector and down-regulated expression of the endogenous c-myc gene. IL-3 selectively failed to stimulate expression of the TRE driven c-myc vector in FDMT myc.A1. Augmented TPA dependent vector derived c-myc expression was accompanied by enhanced mitogenesis of the cell line FDMT myc.A1 compared with FDC-P1. In addition, TPA mediated expression of the transfected c-myc gene in FDMT myc.A1 was accompanied by augmented transcription of c-jun and c-fos in response to TPA. These studies show the importance of a non-protein kinase C dependent pathway for IL-3 mediated c-myc transcription. However, these studies reveal that protein kinase C mediated pathways can be promitogenic, especially when complemented by unregulated c-myc expression (in this case driven by an alternative, TRE containing promoter).
T S Nahreini; S Litz-Jackson; G S Burgess; L M Helvering; S C Manolagas; H S Boswell
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Leukemia     Volume:  5     ISSN:  0887-6924     ISO Abbreviation:  Leukemia     Publication Date:  1991 Dec 
Date Detail:
Created Date:  1992-03-04     Completed Date:  1992-03-04     Revised Date:  2013-03-04    
Medline Journal Info:
Nlm Unique ID:  8704895     Medline TA:  Leukemia     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1099-109     Citation Subset:  IM    
Department of Medicine, Indiana University School of Medicine, Indianapolis.
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MeSH Terms
Blotting, Northern
Blotting, Southern
Cell Line
Gene Expression Regulation
Genes, jun
Genes, myc
Genetic Vectors
Interleukin-3 / pharmacology*
Mitosis / drug effects
Promoter Regions, Genetic
Protein Kinase C / physiology
RNA, Messenger / genetics
Recombinant Proteins / genetics
Signal Transduction
Tetradecanoylphorbol Acetate / pharmacology
Transcription, Genetic
Grant Support
Reg. No./Substance:
0/Interleukin-3; 0/RNA, Messenger; 0/Recombinant Proteins; 16561-29-8/Tetradecanoylphorbol Acetate; EC Kinase C

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