ArticleCancer science2015
Functional interplay between MYCN, NCYM, and OCT4 promotes aggressiveness of human neuroblastomas.
Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Diagnostic significance and carcinogenic mechanism of pan-cancer gene POU5F1 in liver hepatocellular carcinoma.Cancer medicine · 2020Pooled it
- PP2A activation targets MYCN in neuroblastoma.Cell death & disease · 2026Article
- Oncogenic roles of young human de novo genes and their potential as neoantigens in cancer immunotherapy.Cell genomics · 2025Article
- Targeting Pathways in Neuroblastoma: Advances in Treatment Strategies and Clinical Outcomes.International journal of molecular sciences · 2025Review
- Multifaceted roles of OCT4 in tumor microenvironment: biology and therapeutic implications.Oncogene · 2025Review
- Rab3B Proteins: Cellular Functions, Regulatory Mechanisms, and Potential as a Cancer Therapy Target.Cell biochemistry and biophysics · 2025Review
- NCYM facilitates cell proliferation and invasion in Wilms tumor by regulating SIX1/β-catenin axis.American journal of clinical and experimental urology · 2025Article
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Cellular and molecular mechanisms of asymmetric stem cell division in tissue homeostasis.Genes to cells : devoted to molecular & cellular mechanisms · 2024Review
- Inhibition of OCT4 binding at theFrontiers in oncology · 2024Article
- Evolution and implications of de novo genes in humans.Nature ecology & evolution · 2023Review
- Evaluating the RIST Molecular-Targeted Regimen in a Three-Dimensional Neuroblastoma Spheroid Cell Culture Model.Cancers · 2023Article
- Structural characterization of humanFrontiers in oncology · 2023Article
- The Origins and Functions of De Novo Genes: Against All Odds?Journal of molecular evolution · 2022Review
- Open reading frame dominance indicates protein-coding potential of RNAs.EMBO reports · 2022Article
- Mechanisms involved in selecting and maintaining neuroblastoma cancer stem cell populations, and perspectives for therapeutic targeting.World journal of stem cells · 2021Review
- Secondary Structure of HumanFrontiers in oncology · 2021Article
- Silencing of the Long Noncoding RNA MYCNOS1 Suppresses Activity of MYCN-Amplified Retinoblastoma Without RB1 Mutation.Investigative ophthalmology & visual science · 2020Article
- SP1-induced HOXD-AS1 promotes malignant progression of cholangiocarcinoma by regulating miR-520c-3p/MYCN.Aging · 2020Article
- The PLAGL2/MYCN/miR-506-3p interplay regulates neuroblastoma cell fate and associates with neuroblastoma progression.Journal of experimental & clinical cancer research : CR · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma is a pediatric solid tumor that originates from embryonic neural crest cells. The MYCN gene locus is frequently amplified in unfavorable neuroblastomas, and the gene product promotes the progression of neuroblastomas. However, the molecular mechanisms by which MYCN amplification contributes to stem cell-like states of neuroblastoma remain elusive. In this study, we show that MYCN and its cis-antisense gene, NCYM, form a positive feedback loop with OCT4, a core regulatory gene maintaining a multipotent state of neural stem cells. We previously reported that NCYM is co-amplified with the MYCN gene in primary human neuroblastomas and that the gene product promotes aggressiveness of neuroblastoma by stabilization of MYCN. In 36 MYCN-amplified primary human neuroblastomas, OCT4 mRNA expression was associated with unfavorable prognosis and was correlated with that of NCYM. The OCT4 protein induced both NCYM and MYCN in human neuroblastoma cells, whereas NCYM stabilized MYCN to induce OCT4 and stem cell-related genes, including NANOG, SOX2, and LIN28. In sharp contrast to MYCN, enforced expression of c-MYC did not enhance OCT4 expression in human neuroblastoma cells. All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Knockdown of NCYM or OCT4 inhibited formation of spheres of neuroblastoma cells and promoted asymmetric cell division in MYCN-amplified human neuroblastoma cells. These results suggest that the functional interplay between MYCN, NCYM, and OCT4 contributes to aggressiveness of MYCN-amplified human neuroblastomas.
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