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- W2076451831 abstract "Two groups (Dearth et al. and Ma et al.) examined the role of insulin receptor substrate (IRS) in mouse mammary gland tumorigenesis and metastasis. Dearth et al. used transgenic mice forced to overexpress IRS-1 or IRS-2, or an immortalized but nontumorigenic cell line (MCF-10A) also forced to overexpress one of these two proteins. In the MCF-10A cells, overexpression of either protein caused an increase in phosphorylation (and activation) of Akt and an increase in proliferation in response to insulin growth factor-1 (IGF-1). Only the IRS-1-overexpressing cells showed enhanced phosphorylation of extracellular signal-related kinases 1 and 2. Both IRS proteins disrupted acinar formation in three-dimensional Matrigel cultures, and both IRS proteins coimmunoprecipitated with β-catenin. In the transgenic mice, there was no effect on lactational capacity, but both groups of mice formed tumors in the mammary glands. The IRS-2-overexpressing mice had more rapid tumor formation than did the IRS-1-overexpressing mice; however, IRS-2 was overexpressed to a greater extent than was IRS-1. Both groups exhibited lung metastasis. The histology of the tumors was quite diverse, and many contained cells that were highly differentiated, which is similar to phenotypes associated with activation of β-catenin. In the tumors from the IRS-1- or IRS-2-overexpressing mice, β-catenin coimmunoprecipitated with the IRS proteins, and there was increased abundance of cyclin D, which is encoded by a β-catenin target gene. In the overexpressing MCF-10A cells, IGF-1 stimulated the association between IRS-1 or IRS-2 and β-catenin." @default.
- W2076451831 created "2016-06-24" @default.
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- W2076451831 date "2006-12-05" @default.
- W2076451831 modified "2023-10-18" @default.
- W2076451831 title "IRS Cancer Connection" @default.
- W2076451831 doi "https://doi.org/10.1126/stke.3652006tw417" @default.
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