Source:http://linkedlifedata.com/resource/pubmed/id/16508948
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2006-4-3
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| pubmed:abstractText |
Active metabolites of vitamin A and D are well known to act as growth inhibitors in hormone-related prostate and breast cancers. When various concentrations of 1alpha,25-dihydroxyvitamin D3 (vitamin D3), all-trans-retinoic acid (ATRA) and 9-cis retinoic acid (9-cis RA) were examined, the androgen-stimulated growth of mouse mammary carcinoma SC-3 cells was inhibited by vitamin D3 alone in a dose-dependent manner. A flow cytometer analysis showed that vitamin D3 leads SC-3 cells to relative G1-growth arrest after 72 h. Characterization of vitamin D3-responsive genes using an oligonucleotide microarray demonstrated that 220 genes were upregulated at more than threefold, and 84 genes were downregulated to less than one-third, compared with the testosterone-stimulated SC-3 cells. Neither cyclin-dependent kinase inhibitors (CDKIs) nor the antiapoptotic bcl-2 gene were induced in vitamin D3-responsive genes, with the exception of a slight induction of p15(INK4B). Importantly, fgf8 was markedly repressed in response to vitamin D3. The exogenous addition of FGF8 canceled the growth suppression by vitamin D3 in SC-3 cells, suggesting that the repression of fgf8 is an indispensable step in vitamin D3-mediated growth inhibition. In reporter assays using the ARE-containing artificial construct and the natural androgen-regulated PSA promoter, co-transfection of the vitamin D receptor (VDR) and androgen receptor (AR) suppressed AR-stimulated promoter activity. In addition, vitamin D3 also suppressed androgen-stimulated promoter activity in the stably transfected SC-3 cells. Moreover, VDR repressed the core promoter activity of fgf8 in COS1 cells and in the SC-3 cells. All these findings strongly suggest that vitamin D3 serves as a negative regulator for both androgen-related and fgf8 transcriptions.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
0021-9541
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2006 Wiley-Liss, Inc.
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| pubmed:issnType |
Print
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| pubmed:volume |
207
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
793-9
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16508948-Androgens,
pubmed-meshheading:16508948-Animals,
pubmed-meshheading:16508948-Breast Neoplasms,
pubmed-meshheading:16508948-Cell Line,
pubmed-meshheading:16508948-Cell Proliferation,
pubmed-meshheading:16508948-Cercopithecus aethiops,
pubmed-meshheading:16508948-Cholecalciferol,
pubmed-meshheading:16508948-Down-Regulation,
pubmed-meshheading:16508948-Fibroblast Growth Factor 8,
pubmed-meshheading:16508948-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16508948-Mammary Glands, Animal,
pubmed-meshheading:16508948-Mice,
pubmed-meshheading:16508948-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:16508948-Promoter Regions, Genetic,
pubmed-meshheading:16508948-Transcription, Genetic,
pubmed-meshheading:16508948-Tretinoin
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| pubmed:year |
2006
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| pubmed:articleTitle |
Vitamin D3 suppresses the androgen-stimulated growth of mouse mammary carcinoma SC-3 cells by transcriptional repression of fibroblast growth factor 8.
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| pubmed:affiliation |
Department of Pathology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
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| pubmed:publicationType |
Journal Article
|