| pubmed-article:16508948 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0678222 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0008318 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0287829 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:16508948 | lifeskim:mentions | umls-concept:C0920533 | lld:lifeskim |
| pubmed-article:16508948 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16508948 | pubmed:dateCreated | 2006-4-3 | lld:pubmed |
| pubmed-article:16508948 | 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. | lld:pubmed |
| pubmed-article:16508948 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16508948 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16508948 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16508948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16508948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16508948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16508948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16508948 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16508948 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16508948 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:16508948 | pubmed:author | pubmed-author:TanakaAkiraA | lld:pubmed |
| pubmed-article:16508948 | pubmed:author | pubmed-author:KamiakitoTomo... | lld:pubmed |
| pubmed-article:16508948 | pubmed:author | pubmed-author:TakayashikiNo... | lld:pubmed |
| pubmed-article:16508948 | pubmed:author | pubmed-author:KawataHirotos... | lld:pubmed |
| pubmed-article:16508948 | pubmed:copyrightInfo | Copyright 2006 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:16508948 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16508948 | pubmed:volume | 207 | lld:pubmed |
| pubmed-article:16508948 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16508948 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16508948 | pubmed:pagination | 793-9 | lld:pubmed |
| pubmed-article:16508948 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:meshHeading | pubmed-meshheading:16508948... | lld:pubmed |
| pubmed-article:16508948 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16508948 | pubmed:articleTitle | Vitamin D3 suppresses the androgen-stimulated growth of mouse mammary carcinoma SC-3 cells by transcriptional repression of fibroblast growth factor 8. | lld:pubmed |
| pubmed-article:16508948 | pubmed:affiliation | Department of Pathology, Jichi Medical University, Shimotsuke, Tochigi, Japan. | lld:pubmed |
| pubmed-article:16508948 | pubmed:publicationType | Journal Article | lld:pubmed |
| entrez-gene:14179 | entrezgene:pubmed | pubmed-article:16508948 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:16508948 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16508948 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16508948 | lld:pubmed |
