| pubmed-article:17260018 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0684249 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1335858 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1422163 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1704858 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C2825965 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0536940 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1413787 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1424110 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C1704241 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0220905 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0332257 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:17260018 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:17260018 | pubmed:issue | 30 | lld:pubmed |
| pubmed-article:17260018 | pubmed:dateCreated | 2007-6-28 | lld:pubmed |
| pubmed-article:17260018 | pubmed:abstractText | Previously, we reported that the paralogous zinc-finger proteins--CTCF and brother of the regulator of imprinted sites (BORIS), directly contribute to transcriptional regulation of NY-ESO-1 in lung cancer cells. To further examine mechanisms that mediate expression of this cancer-testis gene, we performed software-guided analysis of the NY-ESO-1 promoter region, which revealed several potential Sp1-binding motifs. Sequential 5-aza-2'deoxycytidine/depsipeptide FK228 treatment markedly induced BORIS expression and enhanced nuclear translocation of Sp1 in lung cancer cells. Transient transfection assays using promoter-reporter constructs, as well as gel-shift and chromatin immunoprecipitation experiments revealed that NY-ESO-1 promoter activity coincided with occupancy of the proximal Sp1-binding site in lung cancer cells. Mutations within the Sp1 recognition sequence specifically eliminated binding of Sp1 to this motif in vitro, and markedly diminished NY-ESO-1 promoter activity in vivo. siRNA-mediated inhibition of Sp1 expression decreased NY-ESO-1 promoter activity, whereas knock down of CTCF expression augmented NY-ESO-1 transcription in lung cancer cells. Co-immunoprecipitation experiments indicated that Sp1 physically interacts with BORIS but not with CTCF in vivo. Collectively, these findings suggest that BORIS recruits Sp1 to mediate de-repression of NY-ESO-1 during pulmonary carcinogenesis. | lld:pubmed |
| pubmed-article:17260018 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17260018 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17260018 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17260018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17260018 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17260018 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17260018 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:17260018 | pubmed:author | pubmed-author:HoodJ MJM | lld:pubmed |
| pubmed-article:17260018 | pubmed:author | pubmed-author:KanoAA | lld:pubmed |
| pubmed-article:17260018 | pubmed:author | pubmed-author:ChenG AGA | lld:pubmed |
| pubmed-article:17260018 | pubmed:author | pubmed-author:NguyenD MDM | lld:pubmed |
| pubmed-article:17260018 | pubmed:author | pubmed-author:SchrumpD SDS | lld:pubmed |
| pubmed-article:17260018 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17260018 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:17260018 | pubmed:volume | 26 | lld:pubmed |
| pubmed-article:17260018 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17260018 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17260018 | pubmed:pagination | 4394-403 | lld:pubmed |
| pubmed-article:17260018 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:17260018 | pubmed:meshHeading | pubmed-meshheading:17260018... | lld:pubmed |
| pubmed-article:17260018 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17260018 | pubmed:articleTitle | Dynamic transcriptional regulatory complexes including BORIS, CTCF and Sp1 modulate NY-ESO-1 expression in lung cancer cells. | lld:pubmed |
| pubmed-article:17260018 | pubmed:affiliation | Thoracic Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1201, USA. | lld:pubmed |
| pubmed-article:17260018 | pubmed:publicationType | Journal Article | lld:pubmed |
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