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• W2016214889 endingPage "52" @default.
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• W2016214889 abstract "Tumor necrosis factor-alpha (TNF-alpha) exerts many cytological effects on a wide range of cells. TNF-alpha can activate nuclear factor-kappa B (NF-kappa B). Activation of NF-kappa B by TNF-alpha mediates many functions of TNF-alpha. The NF-kappa B inhibitor, I kappa B alpha, negatively regulates the activity of NF-kappa B. In MCF-7 cells (an estrogen and TNF-alpha receptor positive cell line), treatment with 17 beta-estradiol (E(2)) inhibited TNF-alpha-induced NF-kappa B DNA binding activity in the gel retardation assays. But, the level of the I kappa B alpha and the TNF-alpha receptor, TNF-R1, were not obviously affected. The NF-kappa B precursor, NF-kappa B p105, has been shown to be associated with NF-kappa B in the cytoplasm and efficiently blocks its nuclear translocation and activation. Treatment of MCF-7 cells with E(2) increased the level of NF-kappa B p105 protein. The anti-estrogen, 4OH-tamoxifen, treatment inhibited E(2)-induced NF-kappa B p105 expression. Our findings indicate that NF-kappa B p105 plays a role in modulating the functions of TNF-alpha in the estrogen receptor positive breast cancer cells." @default.
• W2016214889 created "2016-06-24" @default.
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• W2016214889 date "2000-12-01" @default.
• W2016214889 modified "2023-09-23" @default.
• W2016214889 title "17β-Estradiol Inhibits Tumor Necrosis Factor-α-Induced Nuclear Factor-κB Activation by Increasing Nuclear Factor-κB p105 Level in MCF-7 Breast Cancer Cells" @default.
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• W2016214889 doi "https://doi.org/10.1006/bbrc.2000.3891" @default.
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