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

Research output: Contribution to journalArticle

47 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)47-52
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume279
Issue number1
DOIs
Publication statusPublished - Dec 9 2000
Externally publishedYes

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Keywords

  • Antigens, CD/metabolism
  • Base Sequence
  • Breast Neoplasms/metabolism
  • DNA Primers
  • Estradiol/pharmacology
  • Humans
  • Hydrolysis
  • NF-kappa B/metabolism
  • Protein Transport
  • Receptors, Tumor Necrosis Factor/metabolism
  • Receptors, Tumor Necrosis Factor, Type I
  • Tamoxifen/analogs & derivatives
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha/antagonists & inhibitors

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