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• W2104462810 abstract "Insulin receptor substrates (IRSs) are signaling adaptors that play a major role in the metabolic and mitogenic actions of insulin and insulin-like growth factors. Reports have recently noted increased levels, or activity, of IRSs in many human cancers, and some have linked this to poor patient prognosis. We found that overexpressed IRS-1 was constitutively phosphorylated in vitro and in vivo and that transgenic mice overexpressing IRS-1 or IRS-2 in the mammary gland showed progressive mammary hyperplasia, tumorigenesis, and metastasis. Tumors showed extensive squamous differentiation, a phenotype commonly seen with activation of the canonical beta-catenin signaling pathway. Consistent with this, IRSs were found to bind beta-catenin in vitro and in vivo. IRS-induced tumorigenesis is unique, given that the IRSs are signaling adaptors with no intrinsic kinase activity, and this supports a growing literature indicating a role for IRSs in cancer. This study defines IRSs as oncogene proteins in vivo and provides new models to develop inhibitors against IRSs for anticancer therapy." @default.
• W2104462810 created "2016-06-24" @default.
• W2104462810 creator A5022098811 @default.
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• W2104462810 creator A5075946064 @default.
• W2104462810 date "2006-12-01" @default.
• W2104462810 modified "2023-10-17" @default.
• W2104462810 title "Mammary Tumorigenesis and Metastasis Caused by Overexpression of Insulin Receptor Substrate 1 (IRS-1) or IRS-2" @default.
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• W2104462810 doi "https://doi.org/10.1128/mcb.00260-06" @default.
• W2104462810 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1698542" @default.
• W2104462810 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17030631" @default.
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