Evidence map›Paper›PMID 23172872›Full record

ArticleGenome research2013

GATA3 acts upstream of FOXA1 in mediating ESR1 binding by shaping enhancer accessibility.

Vasiliki Theodorou, Rory Stark, Suraj Menon, Jason S Carroll

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
241citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

241 citing papers in PubMed, 1 synthesis or guideline pooled it, 377 citations in OpenAlex.

  1. Pooled it
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  4. FFPE-CUTAC: A Single Assay, Multiple Layers.bioRxiv : the preprint server for biology · 2026
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  20. TRIM24 as a therapeutic target in endocrine treatment-resistant breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article

181 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Vasiliki TheodorouNuclear Receptor Transcription Lab, Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge CB2 0RE, United Kingdom.
Rory Stark
Suraj Menon
Jason S Carroll
Cancer Research UK · GBUniversity of Cambridge · GB

Funding

Cancer Research UK 15602
6 · The paper itself

Abstract

Estrogen receptor (ESR1) drives growth in the majority of human breast cancers by binding to regulatory elements and inducing transcription events that promote tumor growth. Differences in enhancer occupancy by ESR1 contribute to the diverse expression profiles and clinical outcome observed in breast cancer patients. GATA3 is an ESR1-cooperating transcription factor mutated in breast tumors; however, its genomic properties are not fully defined. In order to investigate the composition of enhancers involved in estrogen-induced transcription and the potential role of GATA3, we performed extensive ChIP-sequencing in unstimulated breast cancer cells and following estrogen treatment. We find that GATA3 is pivotal in mediating enhancer accessibility at regulatory regions involved in ESR1-mediated transcription. GATA3 silencing resulted in a global redistribution of cofactors and active histone marks prior to estrogen stimulation. These global genomic changes altered the ESR1-binding profile that subsequently occurred following estrogen, with events exhibiting both loss and gain in binding affinity, implying a GATA3-mediated redistribution of ESR1 binding. The GATA3-mediated redistributed ESR1 profile correlated with changes in gene expression, suggestive of its functionality. Chromatin loops at the TFF locus involving ESR1-bound enhancers occurred independently of ESR1 when GATA3 was silenced, indicating that GATA3, when present on the chromatin, may serve as a licensing factor for estrogen-ESR1-mediated interactions between cis-regulatory elements. Together, these experiments suggest that GATA3 directly impacts ESR1 enhancer accessibility, and may potentially explain the contribution of mutant-GATA3 in the heterogeneity of ESR1+ breast cancer.

Indexed as

Enhancer Elements, GeneticTranscription, GeneticCell Line, TumorChromatinChromatin Assembly and DisassemblyEstrogen Receptor alphaEstrogensGATA3 Transcription FactorHepatocyte Nuclear Factor 3-alphaHistonesHumansProtein BindingRNA, Small InterferingTrefoil Factor-1Tumor Suppressor ProteinsChromatinESR1 protein, humanEstrogen Receptor alphaEstrogensFOXA1 protein, humanGATA3 protein, humanGATA3 Transcription FactorHepatocyte Nuclear Factor 3-alphaHistonesRNA, Small InterferingTFF1 protein, humanTrefoil Factor-1Tumor Suppressor Proteins

Identifiers

PMID23172872
PMCPMC3530671
OpenAlexW1990153910

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.