17 beta-estradiol inhibits tumor necrosis factor-alpha-induced nuclear factor-kappa B activation by increasing nuclear factor-kappa B p105 level in MCF-7 breast cancer cells

S M Hsu, Y C Chen, M C Jiang

研究成果: 雜誌貢獻文章同行評審

49 引文 斯高帕斯(Scopus)

摘要

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.
原文英語
頁(從 - 到)47-52
頁數6
期刊Biochemical and Biophysical Research Communications
279
發行號1
DOIs
出版狀態已發佈 - 十二月 9 2000
對外發佈Yes

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