Evidence map›Paper›PMID 31439835›Full record

ArticleNature communications2019

The Eleanor ncRNAs activate the topological domain of the ESR1 locus to balance against apoptosis.

Mohamed Osama Ali Abdalla, Tatsuro Yamamoto, Kazumitsu Maehara, Jumpei Nogami, Yasuyuki Ohkawa, Hisashi Miura, Rawin Poonperm, Ichiro Hiratani, Hideki Nakayama, Mitsuyoshi Nakao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  8. Mechanisms of Long Non-Coding RNA in Breast Cancer.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. ArcRNAs and the formation of nuclear bodies.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Review
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  15. Article
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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

11 authors at 6 institutions in 2 countries.

Mohamed Osama Ali AbdallaDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0002-4153-4696
Tatsuro YamamotoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, 860-0811, Japan.
Kazumitsu MaeharaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
Jumpei NogamiDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
Yasuyuki OhkawaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
Hisashi MiuraLaboratory for Developmental Epigenetics, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, 650-0047, Japan.ORCID http://orcid.org/0000-0003-1270-776X
Rawin PoonpermLaboratory for Developmental Epigenetics, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, 650-0047, Japan.
Ichiro HirataniLaboratory for Developmental Epigenetics, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, 650-0047, Japan.
Hideki NakayamaDepartment of Oral and Maxillofacial Surgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.
Mitsuyoshi NakaoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, 860-0811, Japan. mnakao@gpo.kumamoto-u.ac.jp.
Noriko SaitohDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, 860-0811, Japan. noriko.saito@jfcr.or.jp.
Kyushu University · JPRIKEN Center for Biosystems Dynamics Research · JPThe Cancer Institute Hospital · JPJapan Science and Technology Agency · JPKumamoto University · JPSuez Canal University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MCF7 cells acquire estrogen-independent proliferation after long-term estrogen deprivation (LTED), which recapitulates endocrine therapy resistance. LTED cells can become primed for apoptosis, but the underlying mechanism is largely unknown. We previously reported that Eleanor non-coding RNAs (ncRNAs) upregulate the ESR1 gene in LTED cells. Here, we show that Eleanors delineate the topologically associating domain (TAD) of the ESR1 locus in the active nuclear compartment of LTED cells. The TAD interacts with another transcriptionally active TAD, which is 42.9 Mb away from ESR1 and contains a gene encoding the apoptotic transcription factor FOXO3. Inhibition of a promoter-associated Eleanor suppresses all genes inside the Eleanor TAD and the long-range interaction between the two TADs, but keeps FOXO3 active to facilitate apoptosis in LTED cells. These data indicate a role of ncRNAs in chromatin domain regulation, which may underlie the apoptosis-prone nature of therapy-resistant breast cancer cells and could be good therapeutic targets.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic Agents, HormonalApoptosisAromatase InhibitorsBinding SitesBreast NeoplasmsChromatinDrug Resistance, NeoplasmEpigenesis, GeneticEstrogen Receptor alphaEstrogensFemaleForkhead Box Protein O3Genetic LociHigh-Throughput Nucleotide SequencingHumansAntineoplastic Agents, HormonalAromatase InhibitorsChromatinESR1 protein, humanEstrogen Receptor alphaEstrogensForkhead Box Protein O3FOXO3 protein, humanRNA, Untranslated

Identifiers

PMID31439835
PMCPMC6706407
OpenAlexW2969680561

What OpenQuestion holds

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LicenceCC BY
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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.