ArticleJCI insight2021
Nonredundant, isoform-specific roles of HDAC1 in glioma stem cells.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Selective histone deacetylase inhibition as a therapeutically relevant strategy in H3K27M-glioma.Neuro-oncology · 2026Article
- Recommended Tool Compounds: Isoform- and Class-Specific Histone Deacetylase Inhibitors.ACS pharmacology & translational science · 2026Review
- Repositioning HDAC Inhibitors for Glioma Treatment: Synthesis and Biological Evaluation.ACS omega · 2026Article
- HDAC11 interacts with the NuRD (MTA3) complex to transcriptionally suppress TGFβ1 expression and inhibit hepatocellular carcinoma metastasis.Clinical epigenetics · 2026Article
- Generation and Characterization of Novel Contilisant+Tubastatin a Multitarget Small Molecules Against Glioblastoma.Pharmaceutics · 2025Article
- Neprilysin regulates the progression of glioblastoma: an in-vitro study using siRNA mediated gene silencing and HDAC1 mediated upregulation of neprilysin in U87 MG cells.Molecular and cellular biochemistry · 2025Article
- Epigenetic Regulation of OLIG2 in Glioblastoma: Mechanisms and Therapeutic Targets to Combat Treatment Resistance.Journal of molecular neuroscience : MN · 2025Review
- HDAC Class I Inhibitor Domatinostat Induces Apoptosis Preferentially in Glioma Stem Cells Through p53-Dependent and -Independent Activation of BAX Expression.International journal of molecular sciences · 2025Article
- Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025Review
- Epigenetic Alterations in Glioblastoma Multiforme as Novel Therapeutic Targets: A Scoping Review.International journal of molecular sciences · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- Constructing Cell-Specific Causal Networks of Individual Cells for Depicting Dynamical Biological Processes.Research (Washington, D.C.) · 2025Article
- Paromomycin targets HDAC1-mediated SUMOylation and IGF1R translocation in glioblastoma.Frontiers in pharmacology · 2024Article
- Quisinostat is a brain-penetrant radiosensitizer in glioblastoma.JCI insight · 2023Article
- Glioma Stem Cells Are Sensitized to BCL-2 Family Inhibition by Compromising Histone Deacetylases.International journal of molecular sciences · 2023Article
- Epigenetic and molecular coordination between HDAC2 and SMAD3-SKI regulates essential brain tumour stem cell characteristics.Nature communications · 2023Article
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is characterized by an aberrant yet druggable epigenetic landscape. One major family of epigenetic regulators, the histone deacetylases (HDACs), are considered promising therapeutic targets for GBM due to their repressive influences on transcription. Although HDACs share redundant functions and common substrates, the unique isoform-specific roles of different HDACs in GBM remain unclear. In neural stem cells, HDAC2 is the indispensable deacetylase to ensure normal brain development and survival in the absence of HDAC1. Surprisingly, we find that HDAC1 is the essential class I deacetylase in glioma stem cells, and its loss is not compensated for by HDAC2. Using cell-based and biochemical assays, transcriptomic analyses, and patient-derived xenograft models, we find that knockdown of HDAC1 alone has profound effects on the glioma stem cell phenotype in a p53-dependent manner. We demonstrate marked suppression in tumor growth upon targeting of HDAC1 and identify compensatory pathways that provide insights into combination therapies for GBM. Our study highlights the importance of HDAC1 in GBM and the need to develop isoform-specific drugs.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.