Evidence map›Paper›PMID 35354905›Full record

ArticleOncogene2022

Selective histone methyltransferase G9a inhibition reduces metastatic development of Ewing sarcoma through the epigenetic regulation of NEU1.

Daniel J García-Domínguez, Nabil Hajji, Roser López-Alemany, Sara Sánchez-Molina, Elisabet Figuerola-Bou, Francisco J Morón Civanto, Santiago Rello-Varona, Eduardo Andrés-León, Adrián Benito, Hector C Keun and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Correlation analysis of the impact ofMicrobiology spectrum · 2025
    Article
  4. Unlocking epigenetics for precision treatment of Ewing's sarcoma.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
  5. Review
  6. Article
  7. Histone Methyltransferases G9a/International journal of molecular sciences · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. 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

14 authors at 6 institutions in 2 countries.

Daniel J García-DomínguezInstitute of Biomedicine of Seville (IBiS), Hospital Universitario Virgen del Rocío, CSIC, CIBERONC, Seville, Spain. dgarcia-ibis@us.es.ORCID http://orcid.org/0000-0001-8150-2747
Nabil HajjiDivision of Brain Sciences, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-0695-920X
Roser López-AlemanySarcoma Research Group, Oncobell Program, Bellvitge Biomedical Research Institute, (IDIBELL), L'Hospitalet de Llobregat, CIBERONC, Barcelona, Spain.
Sara Sánchez-MolinaDevelopmental Tumour Biology Laboratory, Hospital Sant Joan de Déu, Barcelona, Spain.ORCID http://orcid.org/0000-0002-1430-131X
Elisabet Figuerola-BouDevelopmental Tumour Biology Laboratory, Hospital Sant Joan de Déu, Barcelona, Spain.ORCID http://orcid.org/0000-0002-6839-9586
Francisco J Morón CivantoInstitute of Biomedicine of Seville (IBiS), Hospital Universitario Virgen del Rocío, CSIC, CIBERONC, Seville, Spain.
Santiago Rello-VaronaSarcoma Research Group, Oncobell Program, Bellvitge Biomedical Research Institute, (IDIBELL), L'Hospitalet de Llobregat, CIBERONC, Barcelona, Spain.ORCID http://orcid.org/0000-0002-7500-5522
Eduardo Andrés-LeónBioinformatics Unit, Instituto de Parasitología y Biomedicina "López-Neyra", Consejo Superior de Investigaciones Científicas (IPBLN-CSIC), Granada, Spain.ORCID http://orcid.org/0000-0002-0621-9914
Adrián BenitoCancer Metabolism and Systems Toxicology Group, Division of Cancer, Imperial College London, London, UK.
Hector C KeunCancer Metabolism and Systems Toxicology Group, Division of Cancer, Imperial College London, London, UK.
Jaume MoraDevelopmental Tumour Biology Laboratory, Hospital Sant Joan de Déu, Barcelona, Spain.
Óscar M TiradoSarcoma Research Group, Oncobell Program, Bellvitge Biomedical Research Institute, (IDIBELL), L'Hospitalet de Llobregat, CIBERONC, Barcelona, Spain.ORCID http://orcid.org/0000-0002-4666-2822
Enrique de Álava *Institute of Biomedicine of Seville (IBiS), Hospital Universitario Virgen del Rocío, CSIC, CIBERONC, Seville, Spain. enrique.alava.sspa@juntadeandalucia.es.ORCID http://orcid.org/0000-0001-8400-046X
Lourdes Hontecillas-Prieto *Institute of Biomedicine of Seville (IBiS), Hospital Universitario Virgen del Rocío, CSIC, CIBERONC, Seville, Spain. lhontecillas-ibis@us.es.ORCID http://orcid.org/0000-0002-0582-3386
Hospital Sant Joan de Déu Barcelona · ESImperial College London · GBInstitut d'Investigació Biomédica de Bellvitge · ESHospital Universitario Virgen Macarena · ESInstituto de Biomedicina de Sevilla · ESConsejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ewing sarcoma (EWS) is an aggressive bone and soft tissue tumor with high susceptibility to metastasize. The underlying molecular mechanisms leading to EWS metastases remain poorly understood. Epigenetic changes have been implicated in EWS tumor growth and progression. Linking epigenetics and metastases may provide insight into novel molecular targets in EWS and improve its treatment. Here, we evaluated the effects of a selective G9a histone methyltransferase inhibitor (BIX01294) on EWS metastatic process. Our results showed that overexpression of G9a in tumors from EWS patients correlates with poor prognosis. Moreover, we observe a significantly higher expression of G9a in metastatic EWS tumor as compared to either primary or recurrent tumor. Using functional assays, we demonstrate that pharmacological G9a inhibition using BIX01294 disrupts several metastatic steps in vitro, such as migration, invasion, adhesion, colony formation and vasculogenic mimicry. Moreover, BIX01294 reduces tumor growth and metastases in two spontaneous metastases mouse models. We further identified the sialidase NEU1 as a direct target and effector of G9a in the metastatic process in EWS. NEU1 overexpression impairs migration, invasion and clonogenic capacity of EWS cell lines. Overall, G9a inhibition impairs metastases in vitro and in vivo through the overexpression of NEU1. G9a has strong potential as a prognostic marker and may be a promising therapeutic target for EWS patients.

Indexed as

Sarcoma, EwingAnimalsCell Line, TumorEpigenesis, GeneticGene Expression Regulation, NeoplasticHistone MethyltransferasesHumansMiceNeoplasm Recurrence, LocalNeuraminidaseOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSHistone MethyltransferasesNEU1 protein, humanNeu1 protein, mouseNeuraminidaseOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWS

Identifiers

PMID35354905
PMCPMC9054661
OpenAlexW4220972502

What Socratic 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 Socratic graph.