Evidence map›Paper›PMID 37976029›Full record

ArticleJournal of neuro-oncology2023

The long non-coding RNA OTX2-AS1 promotes tumor growth and predicts response to BCL-2 inhibition in medulloblastoma.

Nan Qin, Eunice Paisana, Daniel Picard, Gabriel Leprivier, Maike Langini, Carlos Custódia, Rita Cascão, Catleen Conrad, Mirko Peitzsch, Anja Stefanski and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Genome-wide DNA methylation analysis of pediatric medulloblastomas from a Brazilian cohort: an exploratory study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

16 authors at 7 institutions in 2 countries.

Nan QinDepartment of Hematology, Oncology, and Clinical Immunology, Medical Faculty, Heinrich Heine University, University Hospital Düsseldorf, Düsseldorf, Germany. nan.qin@med.uni-duesseldorf.de.
Eunice PaisanaInstituto de Medicina Molecular João Lobo Antunes (iMM), Faculdade de Medicina da Universidade de Lisboa, Lisbon, 1649-028, Portugal.
Daniel PicardDepartment of Pediatric Oncology, Hematology, and Clinical Immunology, Medical Faculty, Heinrich Heine University, University Hospital Düsseldorf, Düsseldorf, Germany.
Gabriel LeprivierInstitute of Neuropathology, Medical Faculty, Heinrich Heine University, and University Hospital Düsseldorf, Düsseldorf, Germany.
Maike LanginiInstitute of Clinical Chemistry and Laboratory Medicine, Medical Faculty Carl Gustav Carus, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Carlos CustódiaInstituto de Medicina Molecular João Lobo Antunes (iMM), Faculdade de Medicina da Universidade de Lisboa, Lisbon, 1649-028, Portugal.
Rita CascãoInstituto de Medicina Molecular João Lobo Antunes (iMM), Faculdade de Medicina da Universidade de Lisboa, Lisbon, 1649-028, Portugal.
Catleen ConradInstitute of Clinical Chemistry and Laboratory Medicine, Medical Faculty Carl Gustav Carus, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Mirko PeitzschInstitute of Clinical Chemistry and Laboratory Medicine, Medical Faculty Carl Gustav Carus, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Anja StefanskiMolecular Proteomics Laboratory, Biological and Medical Research Center (BMFZ), Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Kai StühlerMolecular Proteomics Laboratory, Biological and Medical Research Center (BMFZ), Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Ute FischerDepartment of Pediatric Oncology, Hematology, and Clinical Immunology, Medical Faculty, Heinrich Heine University, University Hospital Düsseldorf, Düsseldorf, Germany.
Claudia C FariaInstituto de Medicina Molecular João Lobo Antunes (iMM), Faculdade de Medicina da Universidade de Lisboa, Lisbon, 1649-028, Portugal.
Sascha DietrichDepartment of Hematology, Oncology, and Clinical Immunology, Medical Faculty, Heinrich Heine University, University Hospital Düsseldorf, Düsseldorf, Germany.
Guido ReifenbergerInstitute of Neuropathology, Medical Faculty, Heinrich Heine University, and University Hospital Düsseldorf, Düsseldorf, Germany.
Marc RemkeDepartment of Pediatric Oncology, Hematology, and Clinical Immunology, Medical Faculty, Heinrich Heine University, University Hospital Düsseldorf, Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEUniversity of Lisbon · PTDüsseldorf University Hospital · DETechnische Universität Dresden · DEDeutschen Konsortium für Translationale Krebsforschung · DESaarland University · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePrimary brain tumors are a leading cause of cancer-related death in children, and medulloblastoma is the most common malignant pediatric brain tumor. The current molecular characterization of medulloblastoma is mainly based on protein-coding genes, while little is known about the involvement of long non-coding RNAs (lncRNAs). This study aimed to elucidate the role of the lncRNA OTX2-AS1 in medulloblastoma.

methodsAnalyses of DNA copy number alterations, methylation profiles, and gene expression data were used to characterize molecular alterations of OTX2-AS1 in medulloblastoma tissue samples. In vitro analyses of medulloblastoma cell models and orthotopic in vivo experiments were carried out for functional characterization of OTX2-AS1. High-throughput drug screening was employed to identify pharmacological inhibitors, while proteomics and metabolomics analyses were performed to address potential mechanisms of drug action.

resultsWe detected amplification and consecutive overexpression of OTX2 and OTX2-AS1 in a subset of medulloblastomas. In addition, OTX2-AS1 promoter methylation was linked to OTX2-AS1 expression. OTX2-AS1 knockout reduced medulloblastoma cell viability and cell migration in vitro and prolonged survival in the D283 orthotopic medulloblastoma mouse xenograft model. Pharmacological inhibition of BCL-2 suppressed the growth of OTX2-AS1 overexpressing medulloblastoma cells in vitro.

conclusionsOur study revealed a pro-tumorigenic role of OTX2-AS1 in medulloblastoma and identified BCL-2 inhibition as a potential therapeutic approach to target OTX2-AS1 overexpressing medulloblastoma cells.

Indexed as

Brain NeoplasmsCerebellar NeoplasmsMedulloblastomaRNA, Long NoncodingAnimalsCell Line, TumorCell ProliferationChildGene Expression Regulation, NeoplasticHumansMiceOtx Transcription FactorsProto-Oncogene Proteins c-bcl-2BCL2 protein, humanOTX2 protein, humanOtx Transcription FactorsProto-Oncogene Proteins c-bcl-2RNA, Long NoncodingBCL-2 inhibitorHigh-throughput drug screeningLncRNAMedulloblastomaOTX2-AS1

Identifiers

PMID37976029
PMCPMC10689561
OpenAlexW4388765844

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.