ArticleMolecular cancer2008
Differential effects of class I isoform histone deacetylase depletion and enzymatic inhibition by belinostat or valproic acid in HeLa cells.
Article in Molecular cancer, 2008. 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, 42 citations in OpenAlex.
- Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026Review
- Drug Repositioning for HPV Clade-Specific Cervicouterine Cancer Using the OCTAD Pipeline.International journal of molecular sciences · 2025Article
- Sodium valproate affects the expression of p16Oncology letters · 2024Article
- Dihydrolipoamide dehydrogenase, pyruvate oxidation, and acetylation-dependent mechanisms intersecting drug iatrogenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Sodium Valproate-Induced Chromatin Remodeling.Frontiers in cell and developmental biology · 2021Review
- Management of epigenomic networks entailed in coronavirus infections and COVID-19.Clinical epigenetics · 2020Review
- Impact of HDAC Inhibitors on Protein Quality Control Systems: Consequences for Precision Medicine in Malignant Disease.Frontiers in cell and developmental biology · 2020Review
- Histone Deacetylase Inhibitors as Therapeutic Interventions on Cervical Cancer Induced by Human Papillomavirus.Frontiers in cell and developmental biology · 2020Review
- Combination Therapy With Histone Deacetylase Inhibitors (HDACi) for the Treatment of Cancer: Achieving the Full Therapeutic Potential of HDACi.Frontiers in oncology · 2018Review
- Antiproliferative effects of TSA, PXD‑101 and MS‑275 in A2780 and MCF7 cells: Acetylated histone H4 and acetylated tubulin as markers for HDACi potency and selectivity.Oncology reports · 2017Article
- Butyrate inhibits pro-proliferative miR-92a by diminishing c-Myc-induced miR-17-92a cluster transcription in human colon cancer cells.Molecular cancer · 2015Article
- Chromatin-targeting small molecules cause class-specific transcriptional changes in pancreatic endocrine cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Histone deacetylase 6 and heat shock protein 90 control the functions of Foxp3(+) T-regulatory cells.Molecular and cellular biology · 2011Article
- Chromatin remodeling, cell proliferation and cell death in valproic acid-treated HeLa cells.PloS one · 2011Article
- Epigenetic Targeting of Transforming Growth Factor β Receptor II and Implications for Cancer Therapy.Molecular and cellular pharmacology · 2009Article
- Promising Molecular Targets for Pharmacological Therapy of Neurodegenerative Pathologies.Acta naturaeArticle
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone acetylation is an epigenetic modification involved in the regulation of gene expression, balanced by histone acetyl transferases and histone deacetylase (HDAC) enzymes. HDAC inhibitors (HDACi) induce growth arrest and cell death in transformed cells, and are currently in many clinical cancer trials. The transcriptional response to HDACi is complex, as is the response to HDAC isoform knockdown (KD). Here, we describe for the first time in a human cancer cell line, a transcriptional comparison of treatment by two structurally unrelated HDACi; belinostat and valproic acid with the KD of HDAC1, 2 and 3 isoforms.
resultsHDAC KD showed anti-proliferative effects, although to a lesser extent than HDACi treatment. Moreover, we found a 2-fold increased resistance of HDAC1 knockdown cells to belinostat, suggesting this isoenzyme as a selective target. While both HDACi treatment and individual class I HDAC KD produce significant transcriptional effects, three-times higher for HDACi, the gene-expression profiles of class I HDAC KD compared with that obtained by HDACi treatment exhibited less than 4% of altered genes in common between the two modes of inhibition. Further, cell-specific effects of HDAC KD are evident by comparison with a recent study in a different cell line.
conclusionThe increased resistance to belinostat in response to HDAC1 depletion indicates the possibility of using this isoform as a predictive biomarker of response to HDACi treatment. Further, the transcriptional response to chemical inhibition of HDACs is very different from that of KD of individual class I HDAC isoforms. These data suggest that the anti-tumor effect of HDACi is indeed linked to class I inhibition, but may be more complex than simply targeting individual HDAC enzymes.
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