Source:http://linkedlifedata.com/resource/pubmed/id/12720296
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2003-4-29
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pubmed:abstractText |
Cyclopentenone prostaglandins (CyPGs), derivatives of arachidonic acid, have been suggested to exert growth-inhibitory activity through peroxisome proliferator-activated receptor (PPAR)-dependent and -independent mechanisms. Here we examined various eicosanoids for growth inhibition and found that the terminal derivative of prostaglandin (PG) J(2) metabolism, 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)), and PGA(1) markedly inhibited the growth and induced apoptosis in AGS gastric carcinoma cells. There were no significant increases in cell death and DNA-fragmentation in the cells with overexpression of PPARalpha or PPARgamma, indicating the possibility that 15d-PGJ(2) and PGA(1) induced apoptosis through PPAR-independent pathway. Moreover, 15d-PGJ(2) and PGA(1) activated the c-jun N-terminal kinase (JNK) and caspase-3 activity in dose- and time-dependent manners. To examine further the role of JNK signaling cascades in apoptosis induced by 15d-PGJ(2) and PGA(1), we transfected dominant-negative (DN) mutants of JNK plasmid into the cells to analyze the apoptotic characteristics of cells overexpressing DN-JNK following exposure to 15d-PGJ(2) and PGA(1). Overexpression of DN-JNK significantly repressed both endogenous JNK and caspase-3 activity, and subsequently decreased apoptosis induced by 15d-PGJ(2) and PGA(1). These results suggested that CyPGs, such as 15d-PGJ(2) and PGA(1), activated JNK signaling pathway, and that JNK activation may be involved in 15d-PGJ(2)- and PGA(1)-induced apoptosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/15-deoxy-delta(12,14)-prostaglandin...,
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin D2,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/prostaglandin A1
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0899-1987
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2003 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
16-24
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12720296-Apoptosis,
pubmed-meshheading:12720296-Caspase 3,
pubmed-meshheading:12720296-Caspases,
pubmed-meshheading:12720296-Cell Division,
pubmed-meshheading:12720296-Enzyme Activation,
pubmed-meshheading:12720296-Humans,
pubmed-meshheading:12720296-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:12720296-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12720296-Mutation,
pubmed-meshheading:12720296-Prostaglandin D2,
pubmed-meshheading:12720296-Prostaglandins A,
pubmed-meshheading:12720296-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:12720296-Signal Transduction,
pubmed-meshheading:12720296-Stomach Neoplasms,
pubmed-meshheading:12720296-Transcription Factors,
pubmed-meshheading:12720296-Transfection,
pubmed-meshheading:12720296-Tumor Cells, Cultured
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pubmed:year |
2003
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pubmed:articleTitle |
Involvement of c-jun N-terminal kinase activation in 15-deoxy-delta12,14-prostaglandin J2-and prostaglandin A1-induced apoptosis in AGS gastric epithelial cells.
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pubmed:affiliation |
Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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