| pubmed-article:17043687 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C1512505 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C0034818 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C0140079 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C1514758 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C1710236 | lld:lifeskim |
| pubmed-article:17043687 | lifeskim:mentions | umls-concept:C0205460 | lld:lifeskim |
| pubmed-article:17043687 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:17043687 | pubmed:dateCreated | 2006-11-1 | lld:pubmed |
| pubmed-article:17043687 | pubmed:abstractText | Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The alphaIR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IR-stimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness. | lld:pubmed |
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| pubmed-article:17043687 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17043687 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17043687 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17043687 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17043687 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17043687 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17043687 | pubmed:issn | 0007-0920 | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:HorwitzK BKB | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:YeeDD | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:LangeC ACA | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:ZhangXX | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:RicheyJ BJB | lld:pubmed |
| pubmed-article:17043687 | pubmed:author | pubmed-author:ByronS ASA | lld:pubmed |
| pubmed-article:17043687 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17043687 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:17043687 | pubmed:volume | 95 | lld:pubmed |
| pubmed-article:17043687 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17043687 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17043687 | pubmed:pagination | 1220-8 | lld:pubmed |
| pubmed-article:17043687 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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