ArticleOncotarget2016
The antihypertensive drug hydralazine activates the intrinsic pathway of apoptosis and causes DNA damage in leukemic T cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Impact ofBiomolecules · 2026Article
- Breast Cancer Disparities in African and African-Ancestry Populations: Genetics, Epigenetics, Structural Barriers and Technology-Enabled Solutions.British journal of biomedical science · 2026Review
- Hydralazine Attenuates Lipopolysaccharide-Induced Murine Myocardial Dysfunction by Inhibition of Semicarbazide-Sensitive Amine Oxidase.Antioxidants (Basel, Switzerland) · 2025Article
- Association of hydralazine use with risk of hematologic neoplasms in patients with hypertension: A nationwide population-based cohort study in Taiwan.PLoS medicine · 2025Article
- Recent advances on gene-related DNA methylation in cancer diagnosis, prognosis, and treatment: a clinical perspective.Clinical epigenetics · 2025Review
- Remote Co-Loading of Doxorubicin and Hydralazine into PEGylated Liposomes: In Vitro Anti-Proliferative Effect Against Breast Cancer.Molecules (Basel, Switzerland) · 2025Article
- The Impact of DNA Methylation inMicroorganisms · 2025Article
- Cellular Epigenetic Targets and Epidrugs in Breast Cancer Therapy: Mechanisms, Challenges, and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Drug repurposing: A novel strategy to target cancer stem cells and therapeutic resistance.Genes & diseases · 2024Review
- Current Advances in Breast Cancer: Implications for Developing New Treatment Strategies Through Epi-Drugs on the Road to Modifying the Epigenome.Journal of clinical practice and research · 2023Review
- Review
- Review
- Synergistic combination of doxorubicin with hydralazine, and disulfiram against MCF-7 breast cancer cell line.PloS one · 2023Article
- Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.International journal of molecular sciences · 2022Review
- Epigenetics-Associated Risk Reduction of Hematologic Neoplasms in a Nationwide Cohort Study: The Chemopreventive and Therapeutic Efficacy of Hydralazine.Frontiers in oncology · 2022Article
- Hydralazine and Enzalutamide: Synergistic Partners against Prostate Cancer.Biomedicines · 2021Article
- Simvastatin therapy attenuates memory deficits that associate with brain monocyte infiltration in chronic hypercholesterolemia.NPJ aging and mechanisms of disease · 2021Article
- Hydralazine augmented ultrasound hyperthermia for the treatment of hepatocellular carcinoma.Scientific reports · 2021Article
- Hydralazine and Panobinostat Attenuate Malignant Properties of Prostate Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic therapies have emerged as promising anticancer approaches, since epigenetic modifications play a major role in tumor initiation and progression. Hydralazine, an approved vasodilator and antihypertensive drug, has been recently shown to act as a DNA methylation inhibitor. Even though hydralazine is already tested in clinical cancer trials, its mechanism of antitumor action remains undefined. Here, we show that hydralazine induced caspase-dependent apoptotic cell death in human p53-mutant leukemic T cells. Moreover, we demonstrate that hydralazine triggered the mitochondrial pathway of apoptosis by inducing Bak activation and loss of the mitochondrial membrane potential. Hydralazine treatment further resulted in the accumulation of reactive oxygen species, whereas a superoxide dismutase mimetic inhibited hydralazine-induced cell death. Interestingly, caspase-9-deficient Jurkat cells or Bcl-2- and Bcl-xL-overexpressing cells were strongly resistant to hydralazine treatment, thereby demonstrating the dependence of hydralazine-induced apoptosis on the mitochondrial death pathway. Furthermore, we demonstrate that hydralazine treatment triggered DNA damage which might contribute to its antitumor effect.
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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.