Indole-3-carbinol is a negative regulator of estrogen receptor-alpha signaling in human tumor cells

J Nutr. 2000 Dec;130(12):2927-31. doi: 10.1093/jn/130.12.2927.

Abstract

Estrogen, via its binding to the estrogen receptor (ER), plays an important role in breast cancer cell proliferation and tumor development. Indole-3-carbinol (I3C), a compound occurring naturally in cruciferous vegetables, exhibits a potent antitumor activity via its regulation of estrogen activity and metabolism. This study was designed to determine the effect of I3C on the potential to inhibit the ER-alpha. Using a reporter gene driven by the estrogen receptor, I3C (10-125 micromol/L) significantly repressed the 17ss-estradiol (E2)-activated ER-alpha signaling in a dose-dependent manner. I3C and breast cancer susceptibility gene 1 (BRCA1) synergistically inhibited transcriptional activity of ER-alpha. Moreover, I3C down-regulated the expression of the estrogen-responsive genes, pS2 and cathepsin-D, and up-regulated BRCA1. The inhibitory effects of I3C did not contribute to its cytotoxic effects because these activities were observed at less than toxic concentrations. These results further suggest that antitumor activities of I3C are associated not only with its regulation of estrogen activity and metabolism, but also its modulation of ER transcription activity.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / etiology
  • Breast Neoplasms / genetics*
  • Cathepsin D / drug effects
  • Cathepsin D / genetics
  • Cathepsin D / metabolism
  • Dose-Response Relationship, Drug
  • Down-Regulation / drug effects
  • Estrogen Antagonists / pharmacology*
  • Estrogen Receptor alpha
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Genes, BRCA1 / drug effects
  • Growth Inhibitors / metabolism
  • Humans
  • Indoles / pharmacology*
  • Proteins / drug effects
  • Proteins / genetics
  • Proteins / metabolism
  • Receptors, Estrogen / genetics
  • Receptors, Estrogen / metabolism*
  • Sp1 Transcription Factor / drug effects
  • Sp1 Transcription Factor / genetics
  • Sp1 Transcription Factor / physiology
  • Transcription, Genetic / drug effects
  • Trefoil Factor-1
  • Tumor Cells, Cultured
  • Tumor Suppressor Proteins

Substances

  • Estrogen Antagonists
  • Estrogen Receptor alpha
  • Growth Inhibitors
  • Indoles
  • Proteins
  • Receptors, Estrogen
  • Sp1 Transcription Factor
  • TFF1 protein, human
  • Trefoil Factor-1
  • Tumor Suppressor Proteins
  • indole-3-carbinol
  • Cathepsin D