Evidence map›Paper›PMID 33097530›Full record

ArticleScience advances2020

RING1B recruits EWSR1-FLI1 and cooperates in the remodeling of chromatin necessary for Ewing sarcoma tumorigenesis.

Sara Sánchez-Molina, Elisabet Figuerola-Bou, Enrique Blanco, María Sánchez-Jiménez, Pablo Táboas, Soledad Gómez, Cecilia Ballaré, Daniel J García-Domínguez, Estela Prada, Lourdes Hontecillas-Prieto and 7 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  8. CRISPR-Cas9 knockout screening identifies KIAA1429 as an essential gene in Ewing sarcoma.Journal of experimental & clinical cancer research : CR · 2023
    Article
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  16. Know when to fold 'em: Polycomb complexes in oncogenic 3D genome regulation.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
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  19. 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

17 authors at 5 institutions in 1 country.

Sara Sánchez-MolinaDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain. ssanchez@fsjd.org luciano.dicroce@crg.es jmora@sjdhospitalbarcelona.org.ORCID 0000-0002-1430-131X
Elisabet Figuerola-BouDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0002-6839-9586
Enrique BlancoCenter for Genomic Regulation (CRG), Barcelona Institute of Science and Technology, 08003 Barcelona, Spain.ORCID 0000-0001-6261-7370
María Sánchez-JiménezDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.
Pablo TáboasDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0003-4972-677X
Soledad GómezDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0002-0578-4276
Cecilia BallaréCenter for Genomic Regulation (CRG), Barcelona Institute of Science and Technology, 08003 Barcelona, Spain.ORCID 0000-0002-9442-807X
Daniel J García-DomínguezInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla-CIBERONC, Department of Pathology, 41013 Seville, Spain.ORCID 0000-0001-8150-2747
Estela PradaDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.
Lourdes Hontecillas-PrietoInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla-CIBERONC, Department of Pathology, 41013 Seville, Spain.
Ángel M CarcabosoDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0002-8485-426X
Óscar M TiradoSarcoma Research Group, Laboratori d'Oncologia Molecular, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL)-CIBERONC, L'Hospitalet de Llobregat, 08908 Barcelona, Spain.ORCID 0000-0002-4666-2822
Inmaculada Hernández-MuñozDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0003-3436-9634
Enrique de ÁlavaInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla-CIBERONC, Department of Pathology, 41013 Seville, Spain.ORCID 0000-0001-8400-046X
Cinzia LavarinoDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain.ORCID 0000-0002-9630-3676
Luciano Di CroceCenter for Genomic Regulation (CRG), Barcelona Institute of Science and Technology, 08003 Barcelona, Spain. ssanchez@fsjd.org luciano.dicroce@crg.es jmora@sjdhospitalbarcelona.org.ORCID 0000-0003-3488-6228
Jaume MoraDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain. ssanchez@fsjd.org luciano.dicroce@crg.es jmora@sjdhospitalbarcelona.org.ORCID 0000-0001-5023-9819
Hospital Sant Joan de Déu Barcelona · ESInstituto de Biomedicina de Sevilla · ESUniversitat Pompeu Fabra · ESInstitució Catalana de Recerca i Estudis Avançats · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ewing sarcoma (EwS) is an aggressive tumor that affects adolescents and young adults. EwS is defined by a chromosomal translocation, EWSR1-FLI1 being the most common, that causes genome reprogramming through remodeling of enhancers. Here, we describe an unexpected function of RING1B, which is highly expressed in EwS. While retaining its repressive activity at Polycomb developmental regulated genes, RING1B colocalizes with EWSR1-FLI1 at active enhancers. We demonstrate that RING1B is necessary for the expression of key EWSR1-FLI1 targets by facilitating oncogene recruitment to their enhancers. Knockdown of RING1B impairs growth of tumor xenografts and expression of genes regulated by EWSR1-FLI1 bound enhancers. Pharmacological inhibition of AURKB with AZD1152 increases H2Aub levels causing down-regulation of RING1B/EWSR1-FLI1 common targets. Our findings demonstrate that RING1B is a critical modulator of EWSR1-FLI1-induced chromatin remodeling, and its inhibition is a potential therapeutic strategy for the treatment of these tumors.

Indexed as

ChromatinSarcoma, EwingAdolescentCarcinogenesisCell Line, TumorCell Transformation, NeoplasticChromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticHumansOncogene Proteins, FusionRNA-Binding Protein EWSYoung AdultChromatinEWSR1-FLI1 fusion protein, humanEWSR1 protein, humanOncogene Proteins, FusionRNA-Binding Protein EWS

Identifiers

PMID33097530
PMCPMC7608835
OpenAlexW3094408921

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.