ArticleCellular oncology (Dordrecht, Netherlands)2015
MYCN concurrence with SAHA-induced cell death in human neuroblastoma cells.
Article in Cellular oncology (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- A Phase 1 Trial of Fimepinostat in Children and Adolescents With Relapsed and Refractory Solid and CNS Tumors.Cancer medicine · 2025Article
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Epigenetic Dysregulation inInternational journal of molecular sciences · 2023Review
- Targeting Oncogenic Transcriptional Networks in Neuroblastoma: From N-Myc to Epigenetic Drugs.International journal of molecular sciences · 2021Review
- MYCN in Neuroblastoma: "Old Wine into New Wineskins".Diseases (Basel, Switzerland) · 2021Review
- Histone deacetylase inhibitor chidamide regulates the Wnt/β-catenin pathway by MYCN/DKK3 in B-ALL.Investigational new drugs · 2021Article
- TargetingFrontiers in oncology · 2020Review
- Article
- ING5-mediated antineuroblastoma effects of suberoylanilide hydroxamic acid.Cancer medicine · 2018Article
- 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
- Histone deacetylase inhibitors VPA and TSA induce apoptosis and autophagy in pancreatic cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- The MYCN Protein in Health and Disease.Genes · 2017Review
- Proteome and Acetylome Analysis Identifies Novel Pathways and Targets Regulated by Perifosine in Neuroblastoma.Scientific reports · 2017Article
- Inhibition of histone deacetylases sensitizes glioblastoma cells to lomustine.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- Altered primary chromatin structures and their implications in cancer development.Cellular oncology (Dordrecht, Netherlands) · 2016Review
- Growth-suppressive effect of suberoylanilide hydroxamic acid (SAHA) on human oral cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the past, the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) has been shown to induce apoptosis in several human tumor types, including neuroblastomas. Amplification and over-expression of the MYCN oncogene is a diagnostic hallmark and a poor prognostic indicator in high-risk neuroblastomas. Here, we studied the relationship between MYCN amplification and over-expression and the anti-tumor effect of SAHA to assess whether this drug may serve as a treatment option for high-risk neuroblastomas.
methodsDifferent human neuroblastoma cell lines, over-expressing or not over-expressing MYCN, were used in this study. Targeted knockdown and exogenous over-expression of MYCN were employed to examine correlations between MYCN expression levels and SAHA responses. After various time periods and concentration exposures to the drug, cell viability was measured by MTS assay, and variations in MYCN mRNA and protein levels were assessed by qPCR and Western blotting, respectively.
resultsWe found that SAHA decreased cell viability in all cell lines tested through apoptosis induction, and that SAHA had a stronger effect on cell lines carrying an amplified MYCN gene. A decrease in MYCN mRNA and protein levels was observed in the SAHA treated cell lines. Subsequent silencing and exogenous over-expression of MYCN changed the proliferation rate of the cells, but did not have any significant impact on the effect of SAHA on the viability of the cells. We also found that SAHA blocked the expression of MYCN and, by doing so, reduced the effects mediated by this protein.
conclusionsOur results suggest that SAHA may be used as a single-drug treatment option for neuroblastomas with an amplified MYCN gene, and as an adjuvant treatment option for all neuroblastomas.
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