| pubmed-article:19070595 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C1367307 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C0007137 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C0036764 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:19070595 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:19070595 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19070595 | pubmed:dateCreated | 2008-12-30 | lld:pubmed |
| pubmed-article:19070595 | pubmed:abstractText | Persistently activated STAT3 contributes to cell survival in many different human cancers. Cancer cell secretion of IL-6 is a frequent basis for persistent STAT3 activation; we show that antibodies against IL-6 or gp-130, the signaling unit of the IL-6 receptor, can abruptly remove persistently activated STAT3 causing prompt disappearance of cysteine proteases of serpin B3/B4 mRNAs, known as squamous cell carcinoma antigens 1 and 2. STAT3 occupies the promoter of serpin B3/B4 before removal and siRNA removal of B3/B4 mRNA caused cell death in HN13 head and neck cancer cells. Thus persistently activated STAT3 is a required part of the continuous activation of B3/B4 genes, which protects tumor cells from dying. | lld:pubmed |
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| pubmed-article:19070595 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19070595 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19070595 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19070595 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19070595 | pubmed:issn | 1090-2104 | lld:pubmed |
| pubmed-article:19070595 | pubmed:author | pubmed-author:DarnellJames... | lld:pubmed |
| pubmed-article:19070595 | pubmed:author | pubmed-author:AhmedSimi TST | lld:pubmed |
| pubmed-article:19070595 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19070595 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:19070595 | pubmed:volume | 378 | lld:pubmed |
| pubmed-article:19070595 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19070595 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19070595 | pubmed:pagination | 821-5 | lld:pubmed |
| pubmed-article:19070595 | pubmed:dateRevised | 2010-9-22 | lld:pubmed |
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| pubmed-article:19070595 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19070595 | pubmed:articleTitle | Serpin B3/B4, activated by STAT3, promote survival of squamous carcinoma cells. | lld:pubmed |
| pubmed-article:19070595 | pubmed:affiliation | Laboratory of Molecular Cell Biology, The Rockefeller University, New York, NY 10065, USA. | lld:pubmed |
| pubmed-article:19070595 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19070595 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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