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cells, irs, cell, igfir, cancer, breast, growth, igfi, receptor, expression, tdya, article, google, scholar, tdyairs, cas, motility, insulin, substrate, insulinlike, data, activation, sfm, proliferation, yee, shown, figure, signalling, human, factor, usa, pathways, mapk, zhang, igfistimulated, lines, tdwt, protein, signaling, treated, proteins, αir, nature, mediate, functional, response, biological, adaptor, clinical, treatment,

Topics {✒️}

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

Questions {❓}

• This raises an important question: what molecular attributes will likely be predictive of tumour dependence on IGF-IR?

Schema {🗺️}

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         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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