Evidence map›Paper›PMID 34850111›Full record

ArticleNucleic acids research2021

A set of accessible enhancers enables the initial response of breast cancer cells to physiological progestin concentrations.

Roser Zaurin, Roberto Ferrari, Ana Silvina Nacht, Jose Carbonell, Francois Le Dily, Jofre Font-Mateu, Lara Isabel de Llobet Cucalon, Enrique Vidal, Antonios Lioutas, Miguel Beato and 1 more

Abstract read
In one paragraph

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. A molecular toolbox to study progesterone receptor signaling.Journal of mammary gland biology and neoplasia · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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.

Roser ZaurinCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Roberto FerrariCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.ORCID 0000-0002-0453-0899
Ana Silvina NachtCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Jose CarbonellCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Francois Le DilyCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.ORCID 0000-0002-8324-7927
Jofre Font-MateuCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Lara Isabel de Llobet CucalonCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Enrique VidalCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.ORCID 0000-0002-4217-1807
Antonios LioutasCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Miguel BeatoCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.
Guillermo P VicentCenter for Genomic Regulation (CRG), Barcelona, 08003, Spain.ORCID 0000-0002-0554-2226

Funding

European Research Council 609989
6 · The paper itself

Abstract

Here, we report that in T47D breast cancer cells 50 pM progestin is sufficient to activate cell cycle entry and the progesterone gene expression program. At this concentration, equivalent to the progesterone blood levels found around the menopause, progesterone receptor (PR) binds only to 2800 genomic sites, which are accessible to ATAC cleavage prior to hormone exposure. These highly accessible sites (HAs) are surrounded by well-organized nucleosomes and exhibit breast enhancer features, including estrogen receptor alpha (ERα), higher FOXA1 and BRD4 (bromodomain containing 4) occupancy. Although HAs are enriched in RAD21 and CTCF, PR binding is the driving force for the most robust interactions with hormone-regulated genes. HAs show higher frequency of 3D contacts among themselves than with other PR binding sites, indicating colocalization in similar compartments. Gene regulation via HAs is independent of classical coregulators and ATP-activated remodelers, relying mainly on MAP kinase activation that enables PR nuclear engagement. HAs are also preferentially occupied by PR and ERα in breast cancer xenografts derived from MCF-7 cells as well as from patients, indicating their potential usefulness as targets for therapeutic intervention.

Indexed as

Enhancer Elements, GeneticGene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationChromatinEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesFemaleHumansMAP Kinase Signaling SystemMCF-7 CellsMiceProgestinsChromatinEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesProgestinsPromegestoneReceptors, Progesterone

Identifiers

PMID34850111
PMCPMC8682742

What OpenQuestion holds

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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.