We are analyzing https://link.springer.com/article/10.1007/s12672-018-0343-8.

Title:
Insulin Receptor Substrate Suppression by the Tyrphostin NT157 Inhibits Responses to Insulin-Like Growth Factor-I and Insulin in Breast Cancer Cells | Discover Oncology
Description:
Insulin and insulin-like growth factor (IGF) signaling systems regulate breast cancer growth, progression, and metastasis. The insulin receptor substrates 1 and 2 (IRS1/2) transduce signaling from the type I IGF receptor (IGF-IR) and insulin receptor (InR) to mediate the biological effects of receptor activation. In breast cancer, IRS-1 plays a critical role in cancer cell proliferation while IRS-2 is associated with motility and metastasis. NT157, a small-molecule tyrphostin, downregulates IRS proteins in several model systems. In breast cancer cells, NT157 treatment suppressed IRS protein expression in a dose-dependent manner. Exposure to NT157 inhibited the activation of downstream signaling mediated by the IRS proteins. NT157 induced a MAPK-dependent serine phosphorylation of IRS proteins which resulted in disassociation between IRS proteins and their receptors resulting in IRS degradation. In estrogen receptor-α-positive (ERα+) breast cancer cells (MCF-7 and T47D), NT157 also resulted in cytoplasmic ERα downregulation likely because of disruption of an IRS-1-IGF-IR/InR/ERα complex. NT157 decreased S phase fraction, monolayer, and anchorage-independent growth after IGF/insulin treatment in ERα+ breast cancer cells. NT157 downregulation of IRS protein expression also sensitized ERα+ breast cancer cells to rapamycin. Moreover, NT157 inhibited the growth of tamoxifen-resistant ERα+ breast cancer cells. Given that both IGF-IR and InR play a role in cancer biology, targeting of IRS adaptor proteins may be a more effective strategy to inhibit the function of these receptors.
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Keywords {🔍}

irs, cancer, cells, breast, erα, growth, cell, protein, signaling, mcf, fig, receptor, expression, proteins, data, article, insulin, overnight, treatment, levels, google, scholar, igfi, cas, treated, determined, induced, degradation, lines, cyclin, yee, results, immunoblotting, total, sirna, starved, insulinlike, igfir, effects, proliferation, actin, panels, serumstarved, panel, serine, phosphorylation, resulted, downregulation, monolayer, tamr,

Topics {✒️}

horseradish peroxidase-conjugated anti-phosphotyrosine disrupt igf-ir/ir-irs-1-erα complex irs-1-igf-ir/inr complex resulting endocrine-resistant breast cancer irs-1-igf-ir/inr/erα complex hormone-resistant tamr cancers mcf-7l tamoxifen-resistant independent triplicates experiments estrogen receptor-α-positive anti-igf-ir-targeted therapies igf-i-stimulated cyclin d1 viola-villegas nt igf-ir monoclonal antibody erα-negative breast cancers irs-igf-ir/inr complex er-positive breast cancers anchorage-independent growth assays ligand-induced erα phosphorylation affect short-term igf transit-siquest transfection reagent masonic cancer center erα + breast cancer cells treatment-induced signaling transduction jie ying chan estrogen receptor alpha insulin receptor substrate insulin receptor substrate-1 insulin receptor substrate-2 nt157 inhibited igf-ir mapk-dependent serine phosphorylation growth factor-mediated signaling small-molecule tyrphostin targeting obesity-induced insulin resistance mediate igf/insulin signaling estrogen-depleted growth media estrogen receptor-positive propidium iodide-stained nuclei igf-i-treated conditions targeting igf-ir axis insulin receptor substrates erα-regulated gene expression erα+ cell lines human breast cancer dose-response curves showed related subjects igf-ir/ir required phospho-igf-ir/ir nt157 binds igf-1r irs-1-igf-ir/ir douglas yee

Questions {❓}

Yee D (2012) Insulin-like growth factor receptor inhibitors: baby or the bathwater?

Schema {🗺️}

WebPage:
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         headline:Insulin Receptor Substrate Suppression by the Tyrphostin NT157 Inhibits Responses to Insulin-Like Growth Factor-I and Insulin in Breast Cancer Cells
         description:Insulin and insulin-like growth factor (IGF) signaling systems regulate breast cancer growth, progression, and metastasis. The insulin receptor substrates 1 and 2 (IRS1/2) transduce signaling from the type I IGF receptor (IGF-IR) and insulin receptor (InR) to mediate the biological effects of receptor activation. In breast cancer, IRS-1 plays a critical role in cancer cell proliferation while IRS-2 is associated with motility and metastasis. NT157, a small-molecule tyrphostin, downregulates IRS proteins in several model systems. In breast cancer cells, NT157 treatment suppressed IRS protein expression in a dose-dependent manner. Exposure to NT157 inhibited the activation of downstream signaling mediated by the IRS proteins. NT157 induced a MAPK-dependent serine phosphorylation of IRS proteins which resulted in disassociation between IRS proteins and their receptors resulting in IRS degradation. In estrogen receptor-α-positive (ERα+) breast cancer cells (MCF-7 and T47D), NT157 also resulted in cytoplasmic ERα downregulation likely because of disruption of an IRS-1-IGF-IR/InR/ERα complex. NT157 decreased S phase fraction, monolayer, and anchorage-independent growth after IGF/insulin treatment in ERα+ breast cancer cells. NT157 downregulation of IRS protein expression also sensitized ERα+ breast cancer cells to rapamycin. Moreover, NT157 inhibited the growth of tamoxifen-resistant ERα+ breast cancer cells. Given that both IGF-IR and InR play a role in cancer biology, targeting of IRS adaptor proteins may be a more effective strategy to inhibit the function of these receptors.
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            Nt Treatment
            Serine Phosphorylation
            Anaplastic Lymphoma Receptor Tyrosine Kinase
            Multiple Breast Cancer Cell Lines
            Oncology
            Cancer Research
            Surgical Oncology
            Molecular Medicine
            Radiotherapy
            Internal Medicine
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ScholarlyArticle:
      headline:Insulin Receptor Substrate Suppression by the Tyrphostin NT157 Inhibits Responses to Insulin-Like Growth Factor-I and Insulin in Breast Cancer Cells
      description:Insulin and insulin-like growth factor (IGF) signaling systems regulate breast cancer growth, progression, and metastasis. The insulin receptor substrates 1 and 2 (IRS1/2) transduce signaling from the type I IGF receptor (IGF-IR) and insulin receptor (InR) to mediate the biological effects of receptor activation. In breast cancer, IRS-1 plays a critical role in cancer cell proliferation while IRS-2 is associated with motility and metastasis. NT157, a small-molecule tyrphostin, downregulates IRS proteins in several model systems. In breast cancer cells, NT157 treatment suppressed IRS protein expression in a dose-dependent manner. Exposure to NT157 inhibited the activation of downstream signaling mediated by the IRS proteins. NT157 induced a MAPK-dependent serine phosphorylation of IRS proteins which resulted in disassociation between IRS proteins and their receptors resulting in IRS degradation. In estrogen receptor-α-positive (ERα+) breast cancer cells (MCF-7 and T47D), NT157 also resulted in cytoplasmic ERα downregulation likely because of disruption of an IRS-1-IGF-IR/InR/ERα complex. NT157 decreased S phase fraction, monolayer, and anchorage-independent growth after IGF/insulin treatment in ERα+ breast cancer cells. NT157 downregulation of IRS protein expression also sensitized ERα+ breast cancer cells to rapamycin. Moreover, NT157 inhibited the growth of tamoxifen-resistant ERα+ breast cancer cells. Given that both IGF-IR and InR play a role in cancer biology, targeting of IRS adaptor proteins may be a more effective strategy to inhibit the function of these receptors.
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      dateModified:2018-09-18T00:00:00Z
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         Inhibits Insulin Receptor Substrate-1
         Nt Treatment
         Serine Phosphorylation
         Anaplastic Lymphoma Receptor Tyrosine Kinase
         Multiple Breast Cancer Cell Lines
         Oncology
         Cancer Research
         Surgical Oncology
         Molecular Medicine
         Radiotherapy
         Internal Medicine
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      name:Nuri A. Temiz
      affiliation:
            name:University of Minnesota
            address:
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      name:Department of Pharmacology, University of Minnesota, Minneapolis, USA
      name:Masonic Cancer Center, University of Minnesota, Minneapolis, USA
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