| pubmed-article:17621267 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17621267 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:17621267 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:17621267 | lifeskim:mentions | umls-concept:C0205282 | lld:lifeskim |
| pubmed-article:17621267 | lifeskim:mentions | umls-concept:C1655731 | lld:lifeskim |
| pubmed-article:17621267 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17621267 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17621267 | pubmed:dateCreated | 2008-1-10 | lld:pubmed |
| pubmed-article:17621267 | pubmed:abstractText | Interleukin-6 (IL-6) is overexpressed and contributes to tumor cell growth in cholangiocarcinoma. Enforced IL-6 production can alter the expression of specific microRNAs (miRNAs) involved in tumor growth, and moreover can modulate expression of methylation-dependent genes. Thus, we assessed the methylation-dependent regulation of miRNA expression in human malignant cholangiocytes stably transfected to overexpress IL-6. The expression of the methyltransferases DNA methyltransferase enzyme-1 and HASJ4442 was increased by IL-6 overexpression, but was decreased by the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR). Expression profiling identified seven miRNAs that were significantly downregulated by IL-6 overexpression (<0.4-fold) and upregulated (>2-fold) by 5-aza-CdR. One of these, miR-370, is embedded in a CpG island. Although 5-aza-CdR increased miR-370 expression by 2.1-fold in malignant cells, the expression in nonmalignant cells was unchanged. The oncogene mitogen-activated protein kinase kinase kinase 8 (MAP3K8) was identified as a target of miR-370, and its expression was decreased by 5-aza-CdR in cholangiocarcinoma cells. Overexpression of IL-6 reduced miR-370 expression and reinstated MAP3K8 expression in vitro as well as in tumor cell xenografts in vivo. Thus, IL-6 may contribute to tumor growth by modulation of expression of selected miRNAs, such as miR-370. These studies define a mechanism by which inflammation-associated cytokines can epigenetically modulate gene expression and directly contribute to tumor biology. | lld:pubmed |
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| pubmed-article:17621267 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17621267 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17621267 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17621267 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17621267 | pubmed:issn | 1476-5594 | lld:pubmed |
| pubmed-article:17621267 | pubmed:author | pubmed-author:SmithHH | lld:pubmed |
| pubmed-article:17621267 | pubmed:author | pubmed-author:HensonRR | lld:pubmed |
| pubmed-article:17621267 | pubmed:author | pubmed-author:PatelTT | lld:pubmed |
| pubmed-article:17621267 | pubmed:author | pubmed-author:MensJJ | lld:pubmed |
| pubmed-article:17621267 | pubmed:author | pubmed-author:Wehbe-JanekHH | lld:pubmed |
| pubmed-article:17621267 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17621267 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:17621267 | pubmed:volume | 27 | lld:pubmed |
| pubmed-article:17621267 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17621267 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17621267 | pubmed:pagination | 378-86 | lld:pubmed |
| pubmed-article:17621267 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:17621267 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17621267 | pubmed:articleTitle | Epigenetic regulation of microRNA-370 by interleukin-6 in malignant human cholangiocytes. | lld:pubmed |
| pubmed-article:17621267 | pubmed:affiliation | Department of Internal Medicine, Scott and White Clinic, Texas A&M University System Health Science Center College of Medicine, Temple, TX, USA. | lld:pubmed |
| pubmed-article:17621267 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17621267 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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