ArticleOncogene2013
Epigenetic regulation of the neuroblastoma genes, Arid3b and Mycn.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed.
- Comparative ASCL1 Interactome Analysis Reveals CDK2-Cyclin A2 as Suppressors of Differentiation in MYCN-Amplified Neuroblastoma.Molecular cancer research : MCR · 2026Article
- Arid3b suppresses CD8 + T cell infiltration and function in microsatellite-stable colorectal cancer via Runx3.Nature communications · 2026Article
- Serine 89 Phosphorylation Controls Nuclear Localization and Transcriptional Activity of ARID3B.Cells · 2026Article
- Long non-coding RNA RP11-196G11.6 inhibits neuroblastoma progression by regulating the miR-376a-3p/RYBP signaling axis.Oncology letters · 2026Article
- Thoracic metastasis of a pediatric posterior fossa group A ependymoma: a rare case and literature review.World journal of pediatric surgery · 2026Article
- RGS3 acts as a tumor promoter by facilitating the regulation of the TGF-β signaling pathway and promoting EMT in ovarian cancer.Cell death discovery · 2025Article
- Identification of genes associated with testicular germ cell tumor susceptibility through a transcriptome-wide association study.American journal of human genetics · 2025Article
- MYCN as an oncogene in pediatric brain tumors.Frontiers in oncology · 2025Review
- Epigenetic Dysregulation inInternational journal of molecular sciences · 2023Review
- The role of LIN28B in tumor progression and metastasis in solid tumor entities.Oncology research · 2023Review
- Integrative approaches generate insights into the architecture of non-syndromic cleft lip with or without cleft palate.HGG advances · 2021Article
- Article
- The Role of LIN28-International journal of molecular sciences · 2020Review
- Article
- Cancer Stem Cells in Neuroblastoma: Expanding the Therapeutic Frontier.Frontiers in molecular neuroscience · 2019Review
- Reversible LSD1 inhibition with HCI-2509 induces the p53 gene expression signature and disrupts the MYCN signature in high-risk neuroblastoma cells.Oncotarget · 2018Article
- Retinoic acid and TGF-β signalling cooperate to overcome MYCN-induced retinoid resistance.Genome medicine · 2017Article
- ARID3B: a Novel Regulator of the Kaposi's Sarcoma-Associated Herpesvirus Lytic Cycle.Journal of virology · 2016Article
- Sendai virus-mediated expression of reprogramming factors promotes plasticity of human neuroblastoma cells.Cancer science · 2015Article
- Neuroblastoma tyrosine kinase signaling networks involve FYN and LYN in endosomes and lipid rafts.PLoS computational biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AT-rich interaction domain molecule 3B (ARID3B) and MYCN are expressed in a portion of neuroblastoma, and form a combination that has strong oncogenic activity in mouse embryonic fibroblasts (MEFs). Here, we show that this combination can also convert neural stem cells to neuroblastoma-like tumor. To address whether there are common mechanisms regulating the expression of this combination of genes, we examined public repositories of gene expression data and found that although these genes are rarely expressed together, co-expression was observed in a proportion of germ cell tumors (GCTs), in embryonic stem (ES) cells and in testis. These cell types and tissues are related to pluripotency and we show here that in mouse ES cells, Arid3b and Mycn are indeed involved in cell proliferation; the former in avoiding cell death and the latter in driving cell cycle progression. Accordingly, the two genes are induced during somatic cell reprogramming to iPS, and this induction is accompanied by the switching of promoter histone marks from H3K27me3 to H3K4me3. Conversely, the switch from H3K4me3 to H3K27me3 in these genes occurs during the differentiation of neural crest to mature sympathetic ganglia cells. In many, if not most, neuroblastomas these genes carry H3K4me3 marks within their promoters. Thus, a failure of the epigenetic silencing of these genes during development may be an underlying factor responsible for neuroblastoma.
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