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CTCF modulates Estrogen Receptor function through specific chromatin and nuclear matrix interactions.

Elisa Fiorito1, Yogita Sharma1, Siv Gilfillan1

  • 1Breast Cancer Research group, Nordic EMBL Partnership, Centre for Molecular Medicine Norway (NCMM), University of Oslo, P.O. 1137 Blindern, 0318 Oslo, Norway.

Nucleic Acids Research
|September 18, 2016
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Summary
This summary is machine-generated.

CTCF binding to enhancer RNAs modulates estrogen-induced gene transcription in breast cancer cells. This interaction with the nuclear lamina limits Estrogen Receptor (ER) looping, impacting cell proliferation.

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Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Research

Background:

  • Estrogen Receptor (ER) mediates long-range chromatin interactions connecting enhancers to transcription start sites.
  • Molecular mechanisms controlling enhancer output and gene activation remain incompletely understood.

Purpose of the Study:

  • Investigate the role of CTCF in regulating estrogen-induced gene transcription.
  • Elucidate the interplay between CTCF, nuclear lamina, and ER in breast cancer cell proliferation.

Main Methods:

  • Assessed CTCF binding to enhancer RNAs upon estrogen stimulation.
  • Studied the impact of CTCF depletion on gene expression and cell proliferation.
  • Uncovered genomic networks involving nuclear lamina and cell cycle regulator genes.

Main Results:

  • CTCF binding to enhancers prevents ER chromatin binding and hinders enhancer-promoter looping.
  • CTCF depletion increases expression of cell division genes and breast cancer cell proliferation.
  • Estrogen-ER signaling regulates nuclear lamina interactions with chromatin loops.

Conclusions:

  • CTCF and nuclear lamina interplay controls ER target gene transcription.
  • This mechanism significantly impacts breast cancer cell growth rates.
  • Findings reveal novel therapeutic targets for breast cancer treatment.