ArticleCell death & disease2017
Neuroblastoma cells depend on HDAC11 for mitotic cell cycle progression and survival.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation.Cancer cell international · 2026Review
- Hdac11 inhibits apoptosis in zebrafish cells under cold stress via downregulating pdcd6 through its downstream enhancer.Molecular biology reports · 2025Article
- Advancements in Hydrazide-Based HDAC Inhibitors: A Review of Recent Developments and Therapeutic Potential.Journal of medicinal chemistry · 2025Review
- Genetic variants of mHuman genomics · 2025Article
- Emerging frontiers in epigenetic-targeted therapeutics for pediatric neuroblastoma.Frontiers in immunology · 2025Review
- Article
- Emerging therapeutic strategies in cancer therapy by HDAC inhibition as the chemotherapeutic potent and epigenetic regulator.Medical oncology (Northwood, London, England) · 2024Review
- Comparative Structure-Based Virtual Screening Utilizing Optimized AlphaFold Model Identifies Selective HDAC11 Inhibitor.International journal of molecular sciences · 2024Article
- Developing targeted therapies for neuroblastoma by dissecting the effects of metabolic reprogramming on tumor microenvironments and progression.Theranostics · 2024Article
- Emerging role of HDAC11 in skeletal muscle biology.Frontiers in cell and developmental biology · 2024Article
- HDAC11 mediates the ubiquitin-dependent degradation of p53 and inhibits the anti-leukemia effect of PD0166285.Medical oncology (Northwood, London, England) · 2023Article
- Targeting HDAC11 activity by FT895 restricts EV71 replication.Virus research · 2023Article
- HDAC11 is related to breast cancer prognosis and inhibits invasion and proliferation of breast cancer cells.International journal of clinical and experimental pathology · 2023Article
- Clinicopathological characteristics and prognostic significance of HDAC11 protein expression in non-small cell lung cancer: a retrospective study.Translational lung cancer research · 2022Article
- Multi-omic characterization of genome-wide abnormal DNA methylation reveals diagnostic and prognostic markers for esophageal squamous-cell carcinoma.Signal transduction and targeted therapy · 2022Article
- Comprehensive Analysis of the Differential Expression and Prognostic Value of Histone Deacetylases in Glioma.Frontiers in cell and developmental biology · 2022Article
- A novel HDAC11 inhibitor potentiates the tumoricidal effects of cordycepin against malignant peripheral nerve sheath tumor through the Hippo signaling pathway.American journal of cancer research · 2022Article
- Article
- Lysine Fatty Acylation: Regulatory Enzymes, Research Tools, and Biological Function.Frontiers in cell and developmental biology · 2021Review
- Molecular Characterization and Clinical Relevance of Lysine Acetylation Regulators in Urological Cancers.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The number of long-term survivors of high-risk neuroblastoma remains discouraging, with 10-year survival as low as 20%, despite decades of considerable international efforts to improve outcome. Major obstacles remain and include managing resistance to induction therapy, which causes tumor progression and early death in high-risk patients, and managing chemotherapy-resistant relapses, which can occur years after the initial diagnosis. Identifying and validating novel therapeutic targets is essential to improve treatment. Delineating and deciphering specific functions of single histone deacetylases in neuroblastoma may support development of targeted acetylome-modifying therapeutics for patients with molecularly defined high-risk neuroblastoma profiles. We show here that HDAC11 depletion in MYCN-driven neuroblastoma cell lines strongly induces cell death, mostly mediated by apoptotic programs. Genes necessary for mitotic cell cycle progression and cell division were most prominently enriched in at least two of three time points in whole-genome expression data combined from two cell systems, and all nine genes in these functional categories were strongly repressed, including CENPA, KIF14, KIF23 and RACGAP1. Enforced expression of one selected candidate, RACGAP1, partially rescued the induction of apoptosis caused by HDAC11 depletion. High-level expression of all nine genes in primary neuroblastomas significantly correlated with unfavorable overall and event-free survival in patients, suggesting a role in mediating the more aggressive biological and clinical phenotype of these tumors. Our study identified a group of cell cycle-promoting genes regulated by HDAC11, being both predictors of unfavorable patient outcome and essential for tumor cell viability. The data indicate a significant role of HDAC11 for mitotic cell cycle progression and survival of MYCN-amplified neuroblastoma cells, and suggests that HDAC11 could be a valuable drug target.
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