| pubmed-article:19142034 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C2239176 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0151686 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0598934 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C2346501 | lld:lifeskim |
| pubmed-article:19142034 | lifeskim:mentions | umls-concept:C0675838 | lld:lifeskim |
| pubmed-article:19142034 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19142034 | pubmed:dateCreated | 2009-4-2 | lld:pubmed |
| pubmed-article:19142034 | pubmed:abstractText | TAC-101, 4-[3,5-bis(trimethylsilyl)benzamido] benzoic acid, is a synthetic ligand for retinoic acid receptor (RAR)-alpha. Here, we demonstrate the contribution of TAC-101-induced AP-1 interference to stabilization of tumor growth. TAC-101 induced transcriptional activation of RAR, resulting in marked elevation of RARbeta, a representative retinoid response marker, and it also significantly repressed the transcriptional activity of AP-1 in JHH-7 cells. In contrast to JHH-7, JHH-6 is another RARalpha-expressing human hepatocellular carcinoma (HCC) cell line with constitutive activation of AP-1, but it is retinoid insensitive and did not respond to the TAC-101-induced RAR signal. TAC-101 did not inhibit AP-1 activity of the JHH-6 cell line, showing that AP-1 interference by TAC-101 must be in parallel with RAR activation. Interleukin-8 (IL-8), one of the AP-1-regulated factors which correlate with a poor prognosis in HCC patients, was found to be overexpressed in JHH-7 cells. TAC-101 reduced IL-8 production without cytotoxicity and inhibited the progression of HCC in the orthotopic mouse model with decreased tumor IL-8 level. These results suggest that downregulation of the extracellular biomarker for AP-1 interference via the induction of retinoid signals will enhance the pharmacological effect of TAC-101 on HCC and it could be useful as a surrogate biomarker of therapeutic efficacy. | lld:pubmed |
| pubmed-article:19142034 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19142034 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19142034 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19142034 | pubmed:issn | 1423-0380 | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:MurakamiKojiK | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:SugiuraShinS | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:KagechikaHiro... | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:YamamotoYasuj... | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:SugimotoAkiko... | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:MoriTomokoT | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:MasukoNorioN | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:YamasakiYasun... | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:EshimaKokoroK | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:FukayaSatoshi... | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:YokoiHiromiH | lld:pubmed |
| pubmed-article:19142034 | pubmed:author | pubmed-author:HondaShizuS | lld:pubmed |
| pubmed-article:19142034 | pubmed:copyrightInfo | Copyright 2009 S. Karger AG, Basel. | lld:pubmed |
| pubmed-article:19142034 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19142034 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:19142034 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19142034 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19142034 | pubmed:pagination | 1-7 | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:meshHeading | pubmed-meshheading:19142034... | lld:pubmed |
| pubmed-article:19142034 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19142034 | pubmed:articleTitle | Contribution of AP-1 interference induced by TAC-101 to tumor growth suppression in a hepatocellular carcinoma model. | lld:pubmed |
| pubmed-article:19142034 | pubmed:affiliation | Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Tokyo, Japan. | lld:pubmed |
| pubmed-article:19142034 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19142034 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
