Document Detail


Requirement of AP-1 for ceramide-induced apoptosis in human leukemia HL-60 cells.
MedLine Citation:
PMID:  7592995     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ceramide has emerged as a novel lipid mediator in cell proliferation, differentiation, and apoptosis. In this work, we demonstrate that the levels of c-jun mRNA, c-Jun protein, and DNA binding activity of a nuclear transcription factor AP-1 to 12-o-tetradecanoylphorbol 13-acetate responsive elements all increased following treatment with the cell-permeable ceramide, N-acetylsphingosine in human leukemia HL-60 cells. N-Acetylsphingosine (1-10 microM) increased the levels of c-jun mRNA in a dose-dependent manner, and maximal expression was achieved 1 h after treatment. Increase of c-jun expression treated with 5 microM N-acetyldihydrosphingosine, which could not induce apoptosis, was one third of that with 5 microM N-acetylsphingosine. Ceramide-induced growth inhibition and DNA fragmentation were both prevented by treatment with curcumin, 1,7-bis[4-hydroxy-3-methoxy-phenyl]-1,6-heptadiene-3,5-dione (an inhibitor of AP-1 activation), or antisense oligonucleotides for c-jun. These results suggest that the transcription factor AP-1 is critical for apoptosis in HL-60 cells and that an intracellular sphingolipid mediator, ceramide, modulates a signal transduction inducing apoptosis through AP-1 activation.
Authors:
H Sawai; T Okazaki; H Yamamoto; H Okano; Y Takeda; M Tashima; H Sawada; M Okuma; H Ishikura; H Umehara
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  270     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  1995 Nov 
Date Detail:
Created Date:  1995-12-26     Completed Date:  1995-12-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  27326-31     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*,  genetics,  physiology*
Base Sequence
Curcumin / pharmacology
DNA, Neoplasm / genetics,  metabolism
Gene Expression / drug effects
Genes, jun
Humans
Leukemia / genetics,  metabolism*,  pathology*
Molecular Sequence Data
Oligonucleotides, Antisense / genetics,  pharmacology
Proto-Oncogene Proteins c-jun / genetics,  metabolism
RNA, Messenger / genetics,  metabolism
Signal Transduction
Sphingosine / analogs & derivatives*,  pharmacology
Transcription Factor AP-1 / metabolism*
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
0/DNA, Neoplasm; 0/N-acetylsphingosine; 0/Oligonucleotides, Antisense; 0/Proto-Oncogene Proteins c-jun; 0/RNA, Messenger; 0/Transcription Factor AP-1; 123-78-4/Sphingosine; 458-37-7/Curcumin

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


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