ArticleScientific reports2018
Dual role of HDAC10 in lysosomal exocytosis and DNA repair promotes neuroblastoma chemoresistance.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
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- Novel selective indole based histone deacetylase 10 inhibitors as anticancer therapeutics.Scientific reports · 2025Article
- Epidrug screening identifies type I PRMT inhibitors as modulators of lysosomal exocytosis and drug sensitivity in cancers.Cell death & disease · 2025Article
- Histone Deacetylase Inhibitors Promote the Anticancer Activity of Cisplatin: Mechanisms and Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- HDAC10 and its implications in Sézary syndrome pathogenesis.Frontiers in cell and developmental biology · 2025Article
- A protracted war against cancer drug resistance.Cancer cell international · 2024Review
- Chemical Versatility in Catalysis and Inhibition of the Class IIb Histone Deacetylases.Accounts of chemical research · 2024Review
- Chidamide and Oxaliplatin Synergistically Inhibit Colorectal Cancer Growth by Regulating the RPS27A-MDM2-P53 Axis.OncoTargets and therapy · 2023Article
- Aza-SAHA Derivatives Are Selective Histone Deacetylase 10 Chemical Probes That Inhibit Polyamine Deacetylation and Phenocopy HDAC10 Knockout.Journal of the American Chemical Society · 2022Article
- Histone deacetylase-10 liberates spermidine to support polyamine homeostasis and tumor cell growth.The Journal of biological chemistry · 2022Article
- Target deconvolution of HDAC pharmacopoeia reveals MBLAC2 as common off-target.Nature chemical biology · 2022Article
- First Fluorescent Acetylspermidine Deacetylation Assay for HDAC10 Identifies Selective Inhibitors with Cellular Target Engagement.Chembiochem : a European journal of chemical biology · 2022Article
- The paradigm of drug resistance in cancer: an epigenetic perspective.Bioscience reports · 2022Review
- Identification of histone deacetylase 10 (HDAC10) inhibitors that modulate autophagy in transformed cells.European journal of medicinal chemistry · 2022Article
- Comprehensive Analysis of the Differential Expression and Prognostic Value of Histone Deacetylases in Glioma.Frontiers in cell and developmental biology · 2022Article
- Combining APR-246 and HDAC-Inhibitors: A Novel Targeted Treatment Option for Neuroblastoma.Cancers · 2021Article
- CIP2A silencing alleviates doxorubicin resistance in MCF7/ADR cells through activating PP2A and autophagy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Article
- Histone deacetylase 10, a potential epigenetic target for therapy.Bioscience reports · 2021Review
- Pre-Senescence Induction in Hepatoma Cells Favors Hepatitis C Virus Replication and Can Be Used in Exploring Antiviral Potential of Histone Deacetylase Inhibitors.International journal of molecular sciences · 2021Article
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Drug resistance is a leading cause for treatment failure in many cancers, including neuroblastoma, the most common solid extracranial childhood malignancy. Previous studies from our lab indicate that histone deacetylase 10 (HDAC10) is important for the homeostasis of lysosomes, i.e. acidic vesicular organelles involved in the degradation of various biomolecules. Here, we show that depleting or inhibiting HDAC10 results in accumulation of lysosomes in chemotherapy-resistant neuroblastoma cell lines, as well as in the intracellular accumulation of the weakly basic chemotherapeutic doxorubicin within lysosomes. Interference with HDAC10 does not block doxorubicin efflux from cells via P-glycoprotein inhibition, but rather via inhibition of lysosomal exocytosis. In particular, intracellular doxorubicin does not remain trapped in lysosomes but also accumulates in the nucleus, where it promotes neuroblastoma cell death. Our data suggest that lysosomal exocytosis under doxorubicin treatment is important for cell survival and that inhibition of HDAC10 further induces DNA double-strand breaks (DSBs), providing additional mechanisms that sensitize neuroblastoma cells to doxorubicin. Taken together, we demonstrate that HDAC10 inhibition in combination with doxorubicin kills neuroblastoma, but not non-malignant cells, both by impeding drug efflux and enhancing DNA damage, providing a novel opportunity to target chemotherapy resistance.
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