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Title:
Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells | British Journal of Cancer
Description:
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 αIR-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.
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nature portfolio translational research privacy policy inhibit igf-i-stimulated entry nature 318 nature advertising growth factor-i-stimulated proliferation t47d-ya/irs-1 cells exhibited igf-i-stimulated cell proliferation measured igf-i-stimulated motility analysed igf-i-stimulated proliferation establish igf-ir-mediated monolayer mediate igf-ir-stimulated proliferation igf-i-activated igf-ir author information authors 0/ reprints t47d-ya/irs-1 cell clones t47d-ya/irs-2 cell clones induce igf-ir-mediated stimulation igf-ir-stimulated cell motility igf-ir-mediated cell motility igf-i-stimulated proliferation short-interfering rna constructs open bar pr-b-null-cell line investigate igf-ir-mediated proliferation igf-i-stimulated growth triple-negative breast cancer igf-i-stimulated motility mda-mb-231bo cells mda-mb-435 cell lines assessed anchorage-independent growth author correspondence igf-i-stimulated increase igf-ii influencing stability igf-ir stimulated proliferation igf-ir-stimulated proliferation antiprogestin-occupied b-receptors igf-ir signal transduction predict igf-ir dependency growth factor-mediated signaling high progesterone-receptor levels mediating igf-ir action 2 short-interfering rna anti-igf-ir agent igf-ir-mediated motility gold particle-coated coverslips disrupt igf-ir signalling igf-ir-stimulated behaviour
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- This raises an important question: what molecular attributes will likely be predictive of tumour dependence on IGF-IR?
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headline:Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells
description: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 αIR-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.
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headline:Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells
description: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 αIR-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.
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- Profit of https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&term=C%20A%20Lange
- How much income does https://scholar.google.co.uk/scholar?as_q=&num=10&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=%22C%20A%20Lange%22&as_publication=&as_ylo=&as_yhi=&as_allsubj=all&hl=en have?
- How much does https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&term=X%20Zhang bring in each month?
- Profit of https://scholar.google.co.uk/scholar?as_q=&num=10&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=%22X%20Zhang%22&as_publication=&as_ylo=&as_yhi=&as_allsubj=all&hl=en
- How much money does https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&term=D%20Yee generate?
- How much money does https://scholar.google.co.uk/scholar?as_q=&num=10&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=%22D%20Yee%22&as_publication=&as_ylo=&as_yhi=&as_allsubj=all&hl=en generate?
- What are the total earnings of https://s100.copyright.com/AppDispatchServlet?title=Insulin%20receptor%20substrates%20mediate%20distinct%20biological%20responses%20to%20insulin-like%20growth%20factor%20receptor%20activation%20in%20breast%20cancer%20cells&author=S%20A%20Byron%20et%20al&contentID=10.1038%2Fsj.bjc.6603354©right=The%20Author%28s%29&publication=0007-0920&publicationDate=2006-10-17&publisherName=SpringerNature&orderBeanReset=true&oa=CC%20BY-NC-SA?
- What's the monthly income of https://citation-needed.springer.com/v2/references/10.1038/sj.bjc.6603354?format=refman&flavour=citation?
- What is the monthly revenue of https://doi.org/10.1038/s41416-020-01094-y?
- https://doi.org/10.1007/s12672-018-0343-8's financial summary
- How much profit does https://doi.org/10.1007/s13346-018-0551-3 make?
- What are the earnings of https://doi.org/10.1038/s41698-017-0017-y?
- How much profit does https://doi.org/10.1186/s12964-016-0148-8 make?
- Income figures for https://www.protocols.io/
- Monthly income for https://www.natureindex.com/
- How much profit does http://www.naturechina.com generate?
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