ArticleCellular and molecular life sciences : CMLS2011
Histone deacetylase inhibitors augment doxorubicin-induced DNA damage in cardiomyocytes.
Article in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
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- Epigenetic evidence of an Ac/Dc axis by VPA and SAHA.Clinical epigenetics · 2021Article
- Valproic acid influences the expression of genes implicated with hyperglycaemia-induced complement and coagulation pathways.Scientific reports · 2021Article
- A yeast phenomic model for the influence of Warburg metabolism on genetic buffering of doxorubicin.Cancer & metabolism · 2019Article
- Beyond Anthracyclines: Preemptive Management of Cardiovascular Toxicity in the Era of Targeted Agents for Hematologic Malignancies.Current hematologic malignancy reports · 2017Review
- Valproic Acid Induces Endocytosis-Mediated Doxorubicin Internalization and Shows Synergistic Cytotoxic Effects in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2017Article
- Modeling Doxorubicin-Induced Cardiotoxicity in Human Pluripotent Stem Cell Derived-Cardiomyocytes.Scientific reports · 2016Article
- Knockdown of Rad9A enhanced DNA damage induced by trichostatin A in esophageal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Nanog requires BRD4 to maintain murine embryonic stem cell pluripotency and is suppressed by bromodomain inhibitor JQ1 together with Lefty1.Stem cells and development · 2015Article
- BRD4 associates with p53 in DNMT3A-mutated leukemia cells and is implicated in apoptosis by the bromodomain inhibitor JQ1.Cancer medicine · 2013Article
- Safety and feasibility of targeted agent combinations in solid tumours.Nature reviews. Clinical oncology · 2013Review
- Histone deacetylase inhibitors (HDACIs): multitargeted anticancer agents.Biologics : targets & therapy · 2013Article
- Potential non-oncological applications of histone deacetylase inhibitors.American journal of translational research · 2011Article
- The Combination of Metformin and Valproic Acid Has a Greater Anti-tumoral Effect on Prostate Cancer GrowthIn vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors have emerged as a new class of anticancer therapeutics with suberoylanilide hydroxamic acid (Vorinostat) and depsipeptide (Romidepsin) already being approved for clinical use. Numerous studies have identified that histone deacetylase inhibitors will be most effective in the clinic when used in combination with conventional cancer therapies such as ionizing radiation and chemotherapeutic agents. One promising combination, particularly for hematologic malignancies, involves the use of histone deacetylase inhibitors with the anthracycline, doxorubicin. However, we previously identified that trichostatin A can potentiate doxorubicin-induced hypertrophy, the dose-limiting side-effect of the anthracycline, in cardiac myocytes. Here we have the extended the earlier studies and evaluated the effects of combinations of the histone deacetylase inhibitors, trichostatin A, valproic acid and sodium butyrate on doxorubicin-induced DNA double-strand breaks in cardiomyocytes. Using γH2AX as a molecular marker for the DNA lesions, we identified that all of the broad-spectrum histone deacetylase inhibitors tested augment doxorubicin-induced DNA damage. Furthermore, it is evident from the fluorescence photomicrographs of stained nuclei that the histone deacetylase inhibitors also augment doxorubicin-induced hypertrophy. These observations highlight the importance of investigating potential side-effects, in relevant model systems, which may be associated with emerging combination therapies for cancer.
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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 OpenQuestion graph.