Evidence map›Paper›PMID 25223786›Full record

ArticleNucleic acids research2014

The transcriptional co-repressor TLE3 suppresses basal signaling on a subset of estrogen receptor α target genes.

Maïka Jangal, Jean-Philippe Couture, Stéphanie Bianco, Luca Magnani, Hisham Mohammed, Nicolas Gévry

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% of its field
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  5. TRIM56 Promotes White Adipose Tissue Browning to Attenuate Obesity by Degrading TLE3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Polarization of the memory B-cell response.Journal of leukocyte biology · 2025
    Review
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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

6 authors at 2 institutions in 2 countries.

Maïka JangalDépartement de biologie, Faculté des sciences, Université de Sherbrooke, 2500 boulevard de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Jean-Philippe CoutureDépartement de biologie, Faculté des sciences, Université de Sherbrooke, 2500 boulevard de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Stéphanie BiancoDépartement de biologie, Faculté des sciences, Université de Sherbrooke, 2500 boulevard de l'Université, Sherbrooke, Québec J1K 2R1, Canada.
Luca MagnaniDepartment of Surgery and Cancer, Imperial Centre for Translational and Experimental Medecine, Imperial College Hammersmith, London W12 0NN, UK.
Hisham MohammedCancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson way, Cambridge CB2 0RE, UK.
Nicolas GévryDépartement de biologie, Faculté des sciences, Université de Sherbrooke, 2500 boulevard de l'Université, Sherbrooke, Québec J1K 2R1, Canada nicolas.gevry@usherbrooke.ca.
Université de Sherbrooke · CACancer Research UK · GB

Funding

Canadian Institutes of Health Research MOP-97802
6 · The paper itself

Abstract

Chromatin constitutes a repressive barrier to the process of ligand-dependent transcriptional activity of nuclear receptors. Nucleosomes prevent the binding of estrogen receptor α (ERα) in absence of ligand and thus represent an important level of transcriptional regulation. Here, we show that in breast cancer MCF-7 cells, TLE3, a co-repressor of the Groucho/Grg/TLE family, interacts with FoxA1 and is detected at regulatory elements of ERα target genes in absence of estrogen. As a result, the chromatin is maintained in a basal state of acetylation, thus preventing ligand-independent activation of transcription. In absence of TLE3, the basal expression of ERα target genes induced by E2 is increased. At the TFF1 gene, the recruitment of TLE3 to the chromatin is FoxA1-dependent and prevents ERα and RNA polymerase II recruitment to TFF1 gene regulatory elements. Moreover, the interaction of TLE3 with HDAC2 results in the maintenance of acetylation at a basal level. We also provide evidence that TLE3 is recruited at several other regulatory elements of ERα target genes and is probably an important co-regulator of the E2 signaling pathway. In sum, our results describe a mechanism by which TLE3 affects ligand dependency in ERα-regulated gene expression via its binding restricting function and its role in gene regulation by histone acetylation.

Indexed as

Gene Expression RegulationCell LineChromatinCo-Repressor ProteinsEstrogen Receptor alphaHepatocyte Nuclear Factor 3-alphaHistone DeacetylasesHistonesHumansMCF-7 CellsRegulatory Elements, TranscriptionalSignal TransductionTranscription, GeneticChromatinCo-Repressor ProteinsEstrogen Receptor alphaFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaHistone DeacetylasesHistonesTLE3 protein, human

Identifiers

PMID25223786
PMCPMC4191390
OpenAlexW2090992719

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.