ArticleOncology research2022
MYCN Directly Targets NeuroD1 to Promote Cellular Proliferation in Neuroblastoma.
Article in Oncology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- NeuroD1-USP1-MYCN axis drives tumor progression in neuroblastoma.Journal of translational medicine · 2026Article
- MYCN Gene Is Activated by High-Level Expression of Stress-Inducible Isoform of Oct-1 Transcription Factor in Human Neuroblastoma Cells.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2026Article
- STK33 as the functional substrate of miR-454-3p for suppression and apoptosis in neuroblastoma.Molecules and cells · 2024Article
- Rabenosyn-5 suppresses non-small cell lung cancer metastasis via inhibiting CDC42 activity.Cancer gene therapy · 2024Article
- Regulatory roles of insulin growth factor binding protein family in neuroblastoma cell proliferation and differentiation: Potential prognostic biomarkers and therapeutic targets for neuroblastoma.Pediatric discovery · 2024Review
- Developing targeted therapies for neuroblastoma by dissecting the effects of metabolic reprogramming on tumor microenvironments and progression.Theranostics · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NeuroD1 is a neuronal differentiation factor that contains a basic helixloophelix (bHLH) motif. Recently, NeuroD1 was found to be associated with tumorigenesis in neuroblastoma (NB) and is known to promote cell proliferation and migration in these cells. Here we found that MYCN regulates the expression of NeuroD1 in NB cells and that the downregulation of MYCN using short hairpin RNAs (shRNA) results in the inhibition of cellular proliferation in NB cells. Moreover, the phenotype induced by MYCN shRNA was rescued by the exogenous expression of NeuroD1. Chromatin immunoprecipitation (ChIP) assay showed that MYCN directly binds to the E-box element in the NeuroD1 promoter region. In addition, our evaluation of two clinical databases showed that there was a positive correlation between the expression of MYCN and NeuroD1 in NB patients, which supports our in vitro data. In conclusion, this study demonstrates that MYCN-regulated NeuroD1 expression is one of the important mechanisms underlying enhanced cellular proliferation induced by the increase in MYCN expression in NB, and our results provide an important therapeutic target for NB in the future.
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Registered trials
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