ArticleOncogene2014
Histone deacetylase 5 blocks neuroblastoma cell differentiation by interacting with N-Myc.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
The trial behind it
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Inhibition of PTTG1 suppresses proliferation and promotes differentiation of neuroblastoma cells by inducing autophagy.Pediatric surgery international · 2025Article
- Emerging frontiers in epigenetic-targeted therapeutics for pediatric neuroblastoma.Frontiers in immunology · 2025Review
- Multi-Target Inhibitor CUDC-101 Impairs DNA Damage Repair and Enhances Radiation Response in Triple-Negative Breast Cell Line.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Suberoylanilide Hydroxamic Acid Ameliorates Pain Sensitization in Central Neuropathic Pain After Spinal Cord Injury via the HDAC5/NEDD4/SCN9A Axis.Neurochemical research · 2023Article
- MYCN Amplification Is Associated with Reduced Expression of Genes Encoding γ-Secretase Complex and NOTCH Signaling Components in Neuroblastoma.International journal of molecular sciences · 2023Article
- Unraveling the Potential Role of NEDD4-like E3 Ligases in Cancer.International journal of molecular sciences · 2022Review
- Insights Into the Function and Clinical Application of HDAC5 in Cancer Management.Frontiers in oncology · 2021Review
- The class II histone deacetylases as therapeutic targets for Parkinson's disease.Neuronal signaling · 2020Review
- TargetingFrontiers in oncology · 2020Review
- The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020Review
- Histone Deacetylases and Histone Deacetylase Inhibitors in Neuroblastoma.Frontiers in cell and developmental biology · 2020Review
- Role of miRNA in the regulation of cannabidiol-mediated apoptosis in neuroblastoma cells.Oncotarget · 2019Article
- Exosomal hsa-miR199a-3p Promotes Proliferation and Migration in Neuroblastoma.Frontiers in oncology · 2019Article
- MYCN is a novel oncogenic target in adult B-ALL that activates the Wnt/β-catenin pathway by suppressing DKK3.Journal of cellular and molecular medicine · 2018Article
- Epigenetic regulation of neuroblastoma development.Cell and tissue research · 2018Review
- Targeting of epigenetic regulators in neuroblastoma.Experimental & molecular medicine · 2018Review
- Upregulation of LYAR induces neuroblastoma cell proliferation and survival.Cell death and differentiation · 2017Article
- Neuroblastoma cells depend on HDAC11 for mitotic cell cycle progression and survival.Cell death & disease · 2017Article
- The BET bromodomain inhibitor exerts the most potent synergistic anticancer effects with quinone-containing compounds and anti-microtubule drugs.Oncotarget · 2016Article
- MYCN and HDAC5 transcriptionally repress CD9 to trigger invasion and metastasis in neuroblastoma.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The N-Myc oncoprotein induces neuroblastoma, which arises from undifferentiated neuroblasts in the sympathetic nervous system, by modulating gene and protein expression and consequently causing cell differentiation block and cell proliferation. The class IIa histone deacetylase 5 (HDAC5) represses gene transcription, and blocks myoblast, osteoblast and leukemia cell differentiation. Here we showed that N-Myc upregulated HDAC5 expression in neuroblastoma cells. Conversely, HDAC5 repressed the ubiquitin-protein ligase NEDD4 gene expression, increased Aurora A gene expression and consequently upregulated N-Myc protein expression. Genome-wide gene expression analysis and protein co-immunoprecipitation assays revealed that HDAC5 and N-Myc repressed the expression of a common subset of genes by forming a protein complex, whereas HDAC5 and the class III HDAC SIRT2 independently repressed the expression of another common subset of genes without forming a protein complex. Moreover, HDAC5 blocked differentiation and induced proliferation in neuroblastoma cells. Taken together, our data identify HDAC5 as a novel co-factor in N-Myc oncogenesis, and provide the evidence for the potential application of HDAC5 inhibitors in the therapy of N-Myc-induced neuroblastoma and potentially other c-Myc-induced malignancies.
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Registered trials
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.