ArticleCancer research2012
EZH2 Mediates epigenetic silencing of neuroblastoma suppressor genes CASZ1, CLU, RUNX3, and NGFR.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.
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Who cites it
111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- Bibliometric and visualization analysis in the field of epigenetics and glioma (2009-2024).Frontiers in oncology · 2024Pooled it
- Pooled it
- 5-hydroxymethylcytosine deposition mediates Polycomb repressive complex 2 function iniScience · 2026Article
- Integrative bioinformatics analysis unveils neuro-cancer crosstalk-related genes and establishes prognostic risk model in Glioblastoma.Scientific reports · 2026Article
- Synthetic lethality of EZH2 and DNMT Inhibition suppresses neuroblastoma proliferation via MYCN destabilization.BMC cancer · 2025Article
- Identification of hub genes predicting sensitivity to neoadjuvant chemoradiation in locally advanced rectal cancer.Radiology and oncology · 2025Article
- Enhancer zeste homolog 2 (EZH2) targeting by small interfering RNA (siRNA); recent advances and prospect.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Interplay Between the Epigenome, the Microenvironment, and the Immune System in Neuroblastoma.Cancers · 2025Review
- Transcription factor 4 is a key mediator of oncogenesis in neuroblastoma by promoting MYC activity.Molecular oncology · 2025Article
- Sustained cancer-relevant alternative RNA splicing events driven by PRMT5 in high-risk neuroblastoma.Molecular oncology · 2025Article
- Emerging frontiers in epigenetic-targeted therapeutics for pediatric neuroblastoma.Frontiers in immunology · 2025Review
- Combined inhibition of histone methyltransferases EZH2 and DOT1L is an effective therapy for neuroblastoma.Cancer medicine · 2024Article
- CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.The Journal of investigative dermatology · 2024Article
- The transcriptional co-repressor Runx1t1 is essential for MYCN-driven neuroblastoma tumorigenesis.Nature communications · 2024Article
- Effects of transcription factorAnnals of surgical treatment and research · 2024Article
- DNA methylation of imprint control regions associated with Alzheimer's disease in non-Hispanic Blacks and non-Hispanic Whites.Clinical epigenetics · 2024Article
- The Interplay Between HIF-1α and EZH2 in Lung Cancer and Dual-Targeted Drug Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- USP7 Inhibition Suppresses Neuroblastoma Growth via Induction of p53-Mediated Apoptosis and EZH2 and N-Myc Downregulation.International journal of molecular sciences · 2023Article
- Role of non-coding RNAs in neuroblastoma.Cancer gene therapy · 2023Review
51 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Neuroblastoma (NB) is the most common extracranial pediatric solid tumor with an undifferentiated status and generally poor prognosis, but the basis for these characteristics remains unknown. In this study, we show that upregulation of the Polycomb protein histone methyltransferase EZH2, which limits differentiation in many tissues, is critical to maintain the undifferentiated state and poor prognostic status of NB by epigenetic repression of multiple tumor suppressor genes. We identified this role for EZH2 by examining the regulation of CASZ1, a recently identified NB tumor suppressor gene whose ectopic restoration inhibits NB cell growth and induces differentiation. Reducing EZH2 expression by RNA interference-mediated knockdown or pharmacologic inhibiton with 3-deazaneplanocin A increased CASZ1 expression, inhibited NB cell growth, and induced neurite extension. Similarly, EZH2(-/-) mouse embryonic fibroblasts (MEF) displayed 3-fold higher levels of CASZ1 mRNA compared with EZH2(+/+) MEFs. In cells with increased expression of CASZ1, treatment with histone deacetylase (HDAC) inhibitor decreased expression of EZH2 and the Polycomb Repressor complex component SUZ12. Under steady-state conditions, H3K27me3 and PRC2 components bound to the CASZ1 gene were enriched, but this enrichment was decreased after HDAC inhibitor treatment. We determined that the tumor suppressors CLU, NGFR, and RUNX3 were also directly repressed by EZH2 like CASZ1 in NB cells. Together, our findings establish that aberrant upregulation of EZH2 in NB cells silences several tumor suppressors, which contribute to the genesis and maintenance of the undifferentiated phenotype of NB tumors.
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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.