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

Fingerprint

NF-kappa B
Estradiol
Tumor Necrosis Factor-alpha
Chemical activation
Cells
Breast Neoplasms
I-kappa B Proteins
Tumor Necrosis Factor Receptors
MCF-7 Cells
Estrogens
Electrophoretic Mobility Shift Assay
Estrogen Receptors
Assays
Cytoplasm
Gels
Cell Line

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

Cite this

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title = "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",
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.",
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",
author = "Hsu, {S M} and Chen, {Y C} and Jiang, {M C}",
note = "Copyright 2000 Academic Press.",
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AU - Hsu, S M

AU - Chen, Y C

AU - Jiang, M C

N1 - Copyright 2000 Academic Press.

PY - 2000/12/9

Y1 - 2000/12/9

N2 - 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.

AB - 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.

KW - Antigens, CD/metabolism

KW - Base Sequence

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KW - DNA Primers

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KW - Humans

KW - Hydrolysis

KW - NF-kappa B/metabolism

KW - Protein Transport

KW - Receptors, Tumor Necrosis Factor/metabolism

KW - Receptors, Tumor Necrosis Factor, Type I

KW - Tamoxifen/analogs & derivatives

KW - Tumor Cells, Cultured

KW - Tumor Necrosis Factor-alpha/antagonists & inhibitors

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