Source:http://linkedlifedata.com/resource/pubmed/id/20148354
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
2010-5-10
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pubmed:abstractText |
We have previously reported that the increase in c-Jun expression induced by quercetin inhibited androgen receptor (AR) transactivation, and Sp1 was involved in quercetin-mediated downregulation of AR activity. Transient transfection assays in this work revealed that co-expression of c-Jun quenched Sp1-induced production of luciferase activity driven by AR promoter or three copies of Sp1 binding elements in the AR promoter. Moreover, c-Jun repressed AR-mediated luciferase activity via androgen-response elements (AREs) of the hK2 gene, while this suppression could be restored partially by cotransfection of Sp1 expression plasmid. The physical associations of c-Jun, Sp1, and AR induced by quercetin were further demonstrated by co-immunoprecipitation experiments. In addition, quercetin-mediated repression of AR expression and activity was partially reversed by blocking of JNK signaling pathway. These results suggested that c-Jun might play an important role in the suppression of AR expression and activity in the presence of quercetin, and association of a c-Jun/Sp1/AR protein complex induced by quercetin represented a novel mechanism that was involved in down-regulation of the AR function in prostate cancer cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Androgen Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Prostate-Specific Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Quercetin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Androgen,
http://linkedlifedata.com/resource/pubmed/chemical/Sp1 Transcription Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1573-4919
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
339
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
253-62
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:20148354-Androgen Receptor Antagonists,
pubmed-meshheading:20148354-Antioxidants,
pubmed-meshheading:20148354-Blotting, Western,
pubmed-meshheading:20148354-Humans,
pubmed-meshheading:20148354-Immunoprecipitation,
pubmed-meshheading:20148354-Male,
pubmed-meshheading:20148354-Promoter Regions, Genetic,
pubmed-meshheading:20148354-Prostate-Specific Antigen,
pubmed-meshheading:20148354-Prostatic Neoplasms,
pubmed-meshheading:20148354-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:20148354-Quercetin,
pubmed-meshheading:20148354-Receptors, Androgen,
pubmed-meshheading:20148354-Sp1 Transcription Factor,
pubmed-meshheading:20148354-Transcription, Genetic,
pubmed-meshheading:20148354-Transcriptional Activation,
pubmed-meshheading:20148354-Tumor Cells, Cultured
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pubmed:year |
2010
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pubmed:articleTitle |
Suppression of the androgen receptor function by quercetin through protein-protein interactions of Sp1, c-Jun, and the androgen receptor in human prostate cancer cells.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, School of Medicine, Shandong University, 44 Wenhua westroad, 250012 Jinan, China. lyuanhq@sdu.edu.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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