Evidence map›Paper›PMID 25923108›Full record

ArticleNature communications2015

A cluster of noncoding RNAs activates the ESR1 locus during breast cancer adaptation.

Saori Tomita, Mohamed Osama Ali Abdalla, Saori Fujiwara, Haruka Matsumori, Kazumitsu Maehara, Yasuyuki Ohkawa, Hirotaka Iwase, Noriko Saitoh, Mitsuyoshi Nakao

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  6. Article
  7. Phase Separation in Chromatin Organization and Human Diseases.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Genome biology of long non-coding RNAs in humans: A virtual karyotype.Computational and structural biotechnology journal · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Review
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  15. Article
  16. Article
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  18. Article
  19. ArcRNAs and the formation of nuclear bodies.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Review
  20. Review
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

9 authors at 3 institutions in 1 country.

Saori TomitaDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Mohamed Osama Ali AbdallaDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Saori FujiwaraDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Haruka MatsumoriDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Kazumitsu MaeharaDepartment of Advanced Initiative Medicine, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan.
Yasuyuki OhkawaDepartment of Advanced Initiative Medicine, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan.
Hirotaka IwaseDepartment of Breast and Endocrine Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Noriko SaitohDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Mitsuyoshi NakaoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
Kumamoto University · JPKyushu University · JPJapan Science and Technology Agency · JP

Funding

Research Education CoreU54CA118623 · NCI · TUSKEGEE UNIVERSITY · PI Fan Wu · 2005 to 2026
$20.2M
6 · The paper itself

Abstract

Estrogen receptor-α (ER)-positive breast cancer cells undergo hormone-independent proliferation after deprivation of oestrogen, leading to endocrine therapy resistance. Up-regulation of the ER gene (ESR1) is critical for this process, but the underlying mechanisms remain unclear. Here we show that the combination of transcriptome and fluorescence in situ hybridization analyses revealed that oestrogen deprivation induced a cluster of noncoding RNAs that defined a large chromatin domain containing the ESR1 locus. We termed these RNAs as Eleanors (ESR1 locus enhancing and activating noncoding RNAs). Eleanors were present in ER-positive breast cancer tissues and localized at the transcriptionally active ESR1 locus to form RNA foci. Depletion of one Eleanor, upstream (u)-Eleanor, impaired cell growth and transcription of intragenic Eleanors and ESR1 mRNA, indicating that Eleanors cis-activate the ESR1 gene. Eleanor-mediated gene activation represents a new type of locus control mechanism and plays an essential role in the adaptation of breast cancer cells.

Indexed as

Adaptation, PhysiologicalBase SequenceBreast NeoplasmsCarcinomaEstrogen Receptor alphaEstrogensFemaleGene Expression ProfilingGene Expression RegulationHumansIn Situ Hybridization, FluorescenceMCF-7 CellsMolecular Sequence DataResveratrolRNA, UntranslatedStilbenesESR1 protein, humanEstrogen Receptor alphaEstrogensResveratrolRNA, UntranslatedStilbenes

Identifiers

PMID25923108
PMCPMC4421845
OpenAlexW2060857762

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.