pubmed-article:12082548 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C1335877 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C1512505 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:12082548 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:12082548 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:12082548 | pubmed:dateCreated | 2002-6-25 | lld:pubmed |
pubmed-article:12082548 | pubmed:abstractText | In addition to acting as a hematopoietic growth factor, interleukin-4 (IL-4) inhibits growth of some transformed cells in vitro and in vivo. In this study, we show that insulin receptor substrate (IRS)-1, IRS-2, and signal transducer and activator of transcription 6 (STAT6) are phosphorylated following IL-4 treatment in MCF-7 breast cancer cells. STAT6 DNA binding is enhanced by IL-4 treatment. STAT6 activation occurs even after IRS-1 depletion, suggesting the two pathways are independent. To examine the role of STAT6 in IL-4-mediated growth inhibition and apoptosis, a full-length STAT6 cDNA was transfected into MCF-7 cells. Transient overexpression of STAT6 resulted in both cytoplasmic and nuclear expression of the protein, increased DNA binding in response to IL-4, and increased transactivation of an IL-4 responsive promoter. In STAT6-transfected cells, basal proliferation was reduced whereas apoptosis was increased. Finally, stable expression of STAT6 resulted in reduced foci formation compared to vector-transfected cells alone. These results suggest STAT6 is required for IL-4-mediated growth inhibition and induction of apoptosis in human breast cancer cells. | lld:pubmed |
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pubmed-article:12082548 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12082548 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12082548 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12082548 | pubmed:issn | 1522-8002 | lld:pubmed |
pubmed-article:12082548 | pubmed:author | pubmed-author:YeeDouglasD | lld:pubmed |
pubmed-article:12082548 | pubmed:author | pubmed-author:GoochJennifer... | lld:pubmed |
pubmed-article:12082548 | pubmed:author | pubmed-author:ChristyBarbar... | lld:pubmed |
pubmed-article:12082548 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12082548 | pubmed:volume | 4 | lld:pubmed |
pubmed-article:12082548 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12082548 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12082548 | pubmed:pagination | 324-31 | lld:pubmed |
pubmed-article:12082548 | pubmed:dateRevised | 2010-6-25 | lld:pubmed |
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