ArticleCell death & disease2023
Differential regulation of H3K9/H3K14 acetylation by small molecules drives neuron-fate-induction of glioma cell.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Spatial Omics in High-Grade Gliomas: Mapping Immune-Tumor Niches for Precision Therapy.Cancer medicine · 2026Review
- Epigenetic remodeling during UV exposure: high resolution analysis of histone post-translational modifications in a DNA binding protein 2 mutant model.Histochemistry and cell biology · 2026Article
- Compressive stress-driven Piezo1 activation and Rho-ROCK mechanotransduction promote tumor progression via epigenetic mechanical memory.Science advances · 2026Article
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Nuclear Histone 3 Post-Translational Modification Profiling in Whole Cells using Spectral Flow Cytometry.bioRxiv : the preprint server for biology · 2026Article
- Mechanical regulation of metabolism, epigenetics, and their interplay.npj biomedical innovations · 2026Review
- Genetics-guided screening and biological validation identify zeylenol as a promising EGFR inhibitor in glioma.Frontiers in genetics · 2026Article
- Tauroursodeoxycholic Acid Inhibits NF-κB/p300/H3K14ac to Attenuate Microglial Activation in Lipopolysaccharide-treated BV-2 Cells and Mice.Molecular neurobiology · 2025Article
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- Review
- Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.Cell proliferation · 2025Article
- Mechanistic insights into the stimulation of the histone H3K9 methyltransferase Clr4 by proximal H3K14 ubiquitination.Science advances · 2025Article
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- Lysine Acetyltransferase 6 Complexes in Neurodevelopmental Disorders and Different Types of Cancer.Results and problems in cell differentiation · 2025Review
- Quantitation of global histone post-translational modifications reveal anti-inflammatory epigenetic mechanisms of liquiritigenin based on the optimized super-SILAC strategy.Frontiers in cell and developmental biology · 2025Article
- HDAC inhibitor MS275 reprograms metabolism to induce differentiation and suppress proliferation in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Neuronal Differentiation of Human Glioma Cells Induced by Parthenolide Under In Vitro Conditions.Biomedicines · 2024Article
- Reprogramming Glioblastoma Cells into Non-Cancerous Neuronal Cells as a Novel Anti-Cancer Strategy.Cells · 2024Article
- Expression of calpastatin hcast 3-25 and activity of the calpain/calpastatin system in human glioblastoma stem cells: possible involvement of hcast 3-25 in cell differentiation.Frontiers in molecular biosciences · 2024Article
- Research progress on S-palmitoylation modification mediated by the ZDHHC family in glioblastoma.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
25 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiation therapy using small molecules is a promising strategy for improving the prognosis of glioblastoma (GBM). Histone acetylation plays an important role in cell fate determination. Nevertheless, whether histone acetylation in specific sites determines GBM cells fate remains to be explored. Through screening from a 349 small molecule-library, we identified that histone deacetylase inhibitor (HDACi) MS-275 synergized with 8-CPT-cAMP was able to transdifferentiate U87MG GBM cells into neuron-like cells, which were characterized by cell cycle arrest, rich neuron biomarkers, and typical neuron electrophysiology. Intriguingly, acetylation tags of histone 3 at lysine 9 (H3K9ac) were decreased in the promoter of multiple oncogenes and cell cycle genes, while ones of H3K9ac and histone 3 at lysine 14 (H3K14ac) were increased in the promoter of neuron-specific genes. We then compiled a list of genes controlled by H3K9ac and H3K14ac, and proved that it is a good predictive power for pathologic grading and survival prediction. Moreover, cAMP agonist combined with HDACi also induced glioma stem cells (GSCs) to differentiate into neuron-like cells through the regulation of H3K9ac/K14ac, indicating that combined induction has the potential for recurrence-preventive application. Furthermore, the combination of cAMP activator plus HDACi significantly repressed the tumor growth in a subcutaneous GSC-derived tumor model, and temozolomide cooperated with the differentiation-inducing combination to prolong the survival in an orthotopic GSC-derived tumor model. These findings highlight epigenetic reprogramming through H3K9ac and H3K14ac as a novel approach for driving neuron-fate-induction of GBM cells.
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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.