Reprogramming the chromatin landscape: interplay of the estrogen and glucocorticoid receptors at the genomic level

Tina B Miranda, Ty C Voss, Myong-Hee Sung, Songjoon Baek, Sam John, Mary Hawkins, Lars Grøntved, R Louis Schiltz, Gordon L Hager

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Cross-talk between estrogen receptors (ER) and glucocorticoid receptors (GR) has been shown to contribute to the development and progression of breast cancer. Importantly, the ER and GR status in breast cancer cells is a significant factor in determining the outcome of the disease. However, mechanistic details defining the cellular interactions between ER and GR are poorly understood. We investigated genome-wide binding profiles for ER and GR upon coactivation and characterized the status of the chromatin landscape. We describe a novel mechanism dictating the molecular interplay between ER and GR. Upon induction, GR modulates access of ER to specific sites in the genome by reorganization of the chromatin configuration for these elements. Binding to these newly accessible sites occurs either by direct recognition of ER response elements or indirectly through interactions with other factors. The unveiling of this mechanism is important for understanding cellular interactions between ER and GR and may represent a general mechanism for cross-talk between nuclear receptors in human disease.

Original languageEnglish
JournalCancer Research
Volume73
Issue number16
Pages (from-to)5130-9
ISSN0008-5472
DOIs
Publication statusPublished - 2013

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Glucocorticoid Receptors
Cytoplasmic and Nuclear Receptors

Keywords

  • Animals
  • Binding Sites
  • Cell Line
  • Chromatin
  • DNA
  • Genome
  • Mice
  • Protein Binding
  • Receptors, Estrogen
  • Receptors, Glucocorticoid
  • Response Elements

Cite this

Miranda, T. B., Voss, T. C., Sung, M-H., Baek, S., John, S., Hawkins, M., ... Hager, G. L. (2013). Reprogramming the chromatin landscape: interplay of the estrogen and glucocorticoid receptors at the genomic level. Cancer Research, 73(16), 5130-9. https://doi.org/10.1158/0008-5472.CAN-13-0742
Miranda, Tina B ; Voss, Ty C ; Sung, Myong-Hee ; Baek, Songjoon ; John, Sam ; Hawkins, Mary ; Grøntved, Lars ; Schiltz, R Louis ; Hager, Gordon L. / Reprogramming the chromatin landscape : interplay of the estrogen and glucocorticoid receptors at the genomic level. In: Cancer Research. 2013 ; Vol. 73, No. 16. pp. 5130-9.
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abstract = "Cross-talk between estrogen receptors (ER) and glucocorticoid receptors (GR) has been shown to contribute to the development and progression of breast cancer. Importantly, the ER and GR status in breast cancer cells is a significant factor in determining the outcome of the disease. However, mechanistic details defining the cellular interactions between ER and GR are poorly understood. We investigated genome-wide binding profiles for ER and GR upon coactivation and characterized the status of the chromatin landscape. We describe a novel mechanism dictating the molecular interplay between ER and GR. Upon induction, GR modulates access of ER to specific sites in the genome by reorganization of the chromatin configuration for these elements. Binding to these newly accessible sites occurs either by direct recognition of ER response elements or indirectly through interactions with other factors. The unveiling of this mechanism is important for understanding cellular interactions between ER and GR and may represent a general mechanism for cross-talk between nuclear receptors in human disease.",
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Miranda, TB, Voss, TC, Sung, M-H, Baek, S, John, S, Hawkins, M, Grøntved, L, Schiltz, RL & Hager, GL 2013, 'Reprogramming the chromatin landscape: interplay of the estrogen and glucocorticoid receptors at the genomic level', Cancer Research, vol. 73, no. 16, pp. 5130-9. https://doi.org/10.1158/0008-5472.CAN-13-0742

Reprogramming the chromatin landscape : interplay of the estrogen and glucocorticoid receptors at the genomic level. / Miranda, Tina B; Voss, Ty C; Sung, Myong-Hee; Baek, Songjoon; John, Sam; Hawkins, Mary; Grøntved, Lars; Schiltz, R Louis; Hager, Gordon L.

In: Cancer Research, Vol. 73, No. 16, 2013, p. 5130-9.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Reprogramming the chromatin landscape

T2 - interplay of the estrogen and glucocorticoid receptors at the genomic level

AU - Miranda, Tina B

AU - Voss, Ty C

AU - Sung, Myong-Hee

AU - Baek, Songjoon

AU - John, Sam

AU - Hawkins, Mary

AU - Grøntved, Lars

AU - Schiltz, R Louis

AU - Hager, Gordon L

PY - 2013

Y1 - 2013

N2 - Cross-talk between estrogen receptors (ER) and glucocorticoid receptors (GR) has been shown to contribute to the development and progression of breast cancer. Importantly, the ER and GR status in breast cancer cells is a significant factor in determining the outcome of the disease. However, mechanistic details defining the cellular interactions between ER and GR are poorly understood. We investigated genome-wide binding profiles for ER and GR upon coactivation and characterized the status of the chromatin landscape. We describe a novel mechanism dictating the molecular interplay between ER and GR. Upon induction, GR modulates access of ER to specific sites in the genome by reorganization of the chromatin configuration for these elements. Binding to these newly accessible sites occurs either by direct recognition of ER response elements or indirectly through interactions with other factors. The unveiling of this mechanism is important for understanding cellular interactions between ER and GR and may represent a general mechanism for cross-talk between nuclear receptors in human disease.

AB - Cross-talk between estrogen receptors (ER) and glucocorticoid receptors (GR) has been shown to contribute to the development and progression of breast cancer. Importantly, the ER and GR status in breast cancer cells is a significant factor in determining the outcome of the disease. However, mechanistic details defining the cellular interactions between ER and GR are poorly understood. We investigated genome-wide binding profiles for ER and GR upon coactivation and characterized the status of the chromatin landscape. We describe a novel mechanism dictating the molecular interplay between ER and GR. Upon induction, GR modulates access of ER to specific sites in the genome by reorganization of the chromatin configuration for these elements. Binding to these newly accessible sites occurs either by direct recognition of ER response elements or indirectly through interactions with other factors. The unveiling of this mechanism is important for understanding cellular interactions between ER and GR and may represent a general mechanism for cross-talk between nuclear receptors in human disease.

KW - Animals

KW - Binding Sites

KW - Cell Line

KW - Chromatin

KW - DNA

KW - Genome

KW - Mice

KW - Protein Binding

KW - Receptors, Estrogen

KW - Receptors, Glucocorticoid

KW - Response Elements

U2 - 10.1158/0008-5472.CAN-13-0742

DO - 10.1158/0008-5472.CAN-13-0742

M3 - Journal article

C2 - 23803465

VL - 73

SP - 5130

EP - 5139

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 16

ER -