Evidence map›Paper›PMID 38864832›Full record

ArticleNeuro-oncology2024

Super-enhancer-driven IRF2BP2 enhances ALK activity and promotes neuroblastoma cell proliferation.

Yanling Chen, Ran Zhuo, Lichao Sun, Yanfang Tao, Gen Li, Frank Zhu, Yunyun Xu, Jianwei Wang, Zhiheng Li, Juanjuan Yu and 12 more

Abstract read
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In one paragraph

Article in Neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025
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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

22 authors.

Yanling ChenInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Ran ZhuoInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Lichao SunDepartment of Medicinal Chemistry, Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing, China.
Yanfang TaoInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Gen LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Frank ZhuDepartment of Internal Medicine, The Ohio State University, Columbus, Ohio, USA.
Yunyun XuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Jianwei WangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-9765-3264
Zhiheng LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Juanjuan YuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Hongli YinInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Di WuInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Xiaolu LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Fang FangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Yi XieInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Yizhou HuDepartment of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Hairong WangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Chun YangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Lei ShiState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xiaodong WangDepartment of Orthopedics, Children's Hospital of Soochow University, Suzhou, China.
Zimu ZhangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Jian PanInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-0292-5141

Funding

Jiangsu Province's Science and Technology Support Program BE2021657Jiangsu Provincial Health Commission Scientific Research Project ZD2022056National Key R&D Program of China 2022YFC2502700National Natural Science Foundation 81970163Natural Science Foundation of Jiangsu Province BK20220047Science and Technology Development Project of Suzhou City SKJY2021109Suzhou Health Talent Training Project GSWS2020047
6 · The paper itself

Abstract

backgroundSuper-enhancers (SEs) typically govern the expression of critical oncogenes and play a fundamental role in the initiation and progression of cancer. Focusing on genes that are abnormally regulated by SE in cancer may be a new strategy for understanding pathogenesis. In the context of this investigation, we have identified a previously unreported SE-driven gene IRF2BP2 in neuroblastoma (NB).

methodsThe expression and prognostic value of IRF2BP2 were detected in public databases and clinical samples. The effect of IRF2BP2 on NB cell growth and apoptosis was evaluated through in vivo and in vitro functional loss experiments. The molecular mechanism of IRF2BP2 was investigated by the study of chromatin regulatory regions and transcriptome sequencing.

resultsThe sustained high expression of IRF2BP2 results from the activation of a novel SE established by NB master transcription factors MYCN, MEIS2, and HAND2, and they form a new complex that regulates the gene network associated with the proliferation of NB cell populations. We also observed a significant enrichment of the AP-1 family at the binding sites of IRF2BP2. Remarkably, within NB cells, AP-1 plays a pivotal role in shaping the chromatin accessibility landscape, thereby exposing the binding site for IRF2BP2. This orchestrated action enables AP-1 and IRF2BP2 to collaboratively stimulate the expression of the NB susceptibility gene ALK, thereby upholding the highly proliferative phenotype characteristic of NB.

conclusionsOur findings indicate that SE-driven IRF2BP2 can bind to AP-1 to maintain the survival of tumor cells via regulating chromatin accessibility of the NB susceptibility gene ALK.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticNeuroblastomaAnaplastic Lymphoma KinaseAnimalsApoptosisBiomarkers, TumorCell Line, TumorDNA-Binding ProteinsHumansMicePrognosisTranscription FactorsTumor Cells, CulturedXenograft Model Antitumor AssaysALK protein, humanAnaplastic Lymphoma KinaseBiomarkers, TumorDNA-Binding ProteinsIRF2BP2 protein, humanTranscription FactorsAP-1chromatin accessibilityIRF2BP2neuroblastomasuper-enhancer

Identifiers

PMID38864832
PMCPMC11449008

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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.