Evidence map›Paper›PMID 32579929›Full record

ArticleCell reports2020

Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor.

Mei Yang, Ji Hoon Lee, Zhao Zhang, Richard De La Rosa, Mingjun Bi, Yuliang Tan, Yiji Liao, Juyeong Hong, Baowen Du, Yanming Wu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

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  15. Roles of enhancer RNAs in sex hormone-dependent cancers.Journal of cancer research and clinical oncology · 2022
    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

19 authors at 8 institutions in 2 countries.

Mei YangDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Ji Hoon LeeDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Zhao ZhangDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Richard De La RosaDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Mingjun BiDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Yuliang TanHoward Hughes Medical Institute, Department of Medicine, University of California, San Diego, CA 92093, USA.
Yiji LiaoDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Juyeong HongDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Baowen DuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Yanming WuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Jessica ScheirerDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Tao HongDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA; Xiangya School of Medicine, Central South University, Changsha 410008, China.
Wei LiDepartment of Biological Chemistry, University of California, Irvine, Irvine, CA 92697, USA; Division of Biostatistics, Dan L. Duncan Comprehensive Cancer Center and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Teng FeiCollege of Life and Health Sciences, Northeastern University, Shenyang 110819, China.
Chen-Lin HsiehCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Zhijie LiuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Wenbo LiDepartment of Biochemistry and Molecular Biology, McGovern Medical School, University of Texas Health Science Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center and UTHealth, Houston, TX 77030, USA.
Michael G RosenfeldHoward Hughes Medical Institute, Department of Medicine, University of California, San Diego, CA 92093, USA.
Kexin XuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Electronic address: xuk3@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USCentral South University · CNDana-Farber Cancer Institute · USHoward Hughes Medical Institute · USNortheastern University · CNThe University of Texas Health Science Center at Houston · USUniversity of California, Irvine · USUniversity of California, San Diego · US

Funding

Novel Coregulators of Estrogen Receptor in Enhancer-regulated TranscriptionR01GM137009 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LIU, ZHIJIE "JASON" · 2020 to 2023
$1.0M
Polycomb -Independent Functions of EZH2 in Castration Resistant Prostate CancerR00CA178199 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI XU, KEXIN · 2015 to 2017
$498k
NCI NIH HHS R00 CA178199NIGMS NIH HHS R01 GM137009
6 · The paper itself

Abstract

The function of enhancer RNAs (eRNAs) in transcriptional regulation remains obscure. By analyzing the genome-wide nascent transcript profiles in breast cancer cells, we identify a special group of eRNAs that are essential for estrogen-induced transcriptional repression. Using eRNAs of TM4SF1 and EFEMP1 as the paradigms, we find that these RNA molecules not only stabilize promoter-enhancer interactions but also recruit liganded estrogen receptor α (ERα) to particular enhancer regions, facilitate the formation of a functional transcriptional complex, and cause gene silencing. Interestingly, ERα is shown to directly bind with eRNAs by its DNA-binding domain. These eRNAs help with the formation of a specific ERα-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes. Our work demonstrates a complete mechanism underlying the action of eRNAs in modulating and refining the locus-specific transcriptional program.

Indexed as

Enhancer Elements, GeneticCell LineDown-RegulationEstrogen Receptor alphaEstrogensF-Box ProteinsHumansJumonji Domain-Containing Histone DemethylasesModels, BiologicalOpen Reading FramesProtein BindingProtein DomainsRNARNA Polymerase IITranscription, GeneticEstrogen Receptor alphaEstrogensF-Box ProteinsJumonji Domain-Containing Histone DemethylasesKDM2A protein, humanRNARNA Polymerase IIenhancer activity regulationenhancer RNAERα signalingtranscriptional repression

Identifiers

PMID32579929
PMCPMC8564762
OpenAlexW2998594744

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.