Evidence map›Paper›PMID 31373033›Full record

ArticleThe EMBO journal2019

C/EBPα mediates the growth inhibitory effect of progestins on breast cancer cells.

A Silvina Nacht, Roberto Ferrari, Roser Zaurin, Valentina Scabia, José Carbonell-Caballero, Francois Le Dily, Javier Quilez, Alexandra Leopoldi, Cathrin Brisken, Miguel Beato and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  7. A New Diterpenoid of IndonesianMolecules (Basel, Switzerland) · 2023
    Article
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  12. Article
  13. The Importance of Breast Adipose Tissue in Breast Cancer.International journal of molecular sciences · 2020
    Review
  14. Review
  15. Article
  16. Article
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

11 authors at 3 institutions in 2 countries.

A Silvina NachtCenter for Genomic Regulation (CRG), Barcelona, Spain.
Roberto FerrariCenter for Genomic Regulation (CRG), Barcelona, Spain.
Roser ZaurinCenter for Genomic Regulation (CRG), Barcelona, Spain.
Valentina ScabiaSwiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.ORCID 0000-0002-2797-7087
José Carbonell-CaballeroCenter for Genomic Regulation (CRG), Barcelona, Spain.
Francois Le DilyCenter for Genomic Regulation (CRG), Barcelona, Spain.
Javier QuilezCenter for Genomic Regulation (CRG), Barcelona, Spain.
Alexandra LeopoldiCenter for Genomic Regulation (CRG), Barcelona, Spain.
Cathrin BriskenSwiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Miguel BeatoCenter for Genomic Regulation (CRG), Barcelona, Spain.ORCID 0000-0002-2878-2222
Guillermo P VicentCenter for Genomic Regulation (CRG), Barcelona, Spain.ORCID 0000-0002-0554-2226
Barcelona Institute of Science and Technology · ESÉcole Polytechnique Fédérale de Lausanne · CHUniversitat Pompeu Fabra · ES

Funding

Centro de Excelencia Severo Ochoa 2013-2017 SEV-2012-0208Departament d'Innovació Universitat i Empresa (DIUiE)ERC Synergy grant 4DGenome 609989European Research Council 609989Spanish Ministry of Economy and Competitiveness SAF2016-75006P
6 · The paper itself

Abstract

Steroid hormones are key gene regulators in breast cancer cells. While estrogens stimulate cell proliferation, progestins activate a single cell cycle followed by proliferation arrest. Here, we use biochemical and genome-wide approaches to show that progestins achieve this effect via a functional crosstalk with C/EBPα. Using ChIP-seq, we identify around 1,000 sites where C/EBPα binding precedes and helps binding of progesterone receptor (PR) in response to hormone. These regions exhibit epigenetic marks of active enhancers, and C/EBPα maintains an open chromatin conformation that facilitates loading of ligand-activated PR. Prior to hormone exposure, C/EBPα favors promoter-enhancer contacts that assure hormonal regulation of key genes involved in cell proliferation by facilitating binding of RAD21, YY1, and the Mediator complex. Knockdown of C/EBPα disrupts enhancer-promoter contacts and decreases the presence of these architectural proteins, highlighting its key role in 3D chromatin looping. Thus, C/EBPα fulfills a previously unknown function as a potential growth modulator in hormone-dependent breast cancer.

Indexed as

AnimalsBreast NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsEnhancer Elements, GeneticEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMCF-7 CellsMiceNeoplasm TransplantationProgestinsCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCell Cycle ProteinsDNA-Binding ProteinsProgestinsRAD21 protein, humanReceptors, ProgesteroneYY1 protein, humanYY1 Transcription Factorbreast cancerC/EBPαcell proliferationhormone-dependent gene regulationprogesterone receptor

Identifiers

PMID31373033
PMCPMC6745496
OpenAlexW2965970582

What OpenQuestion holds

Textmetadata
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.