ArticleClinical epigenetics2018
The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes.
Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 104 citations in OpenAlex.
- Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancer.Food & function · 2020Trial
- Epigenetic Modulation by Luteolin, Quercetin and Apigenin in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Research progress on active components from natural medicines inhibiting tumor via epigenetic regulation.Molecular biology reports · 2026Review
- Preliminary Effects of Benralizumab in an AML Cell Model with Promyelocytic Features Expressing IL-5R: An Exploratory Proof-of-Concept Study.Biomedicines · 2026Article
- Review
- Nutriepigenetics and nutriepigenomics: Exploring the interactions between nutrition, epigenetics, and epigenomics in the pathogenesis of noncommunicable diseases.Genetics and molecular biology · 2026Article
- Targeting TGF-β-driven fibrotic, epigenetic remodeling and Bax/Bcl-2 through polyphenol-exercise synergy: molecular implications for biomechanical impairment and rehabilitation in cancer.Frontiers in oncology · 2026Review
- Epigenetic drugs in cancer therapy: mechanisms, immune modulation, and therapeutic applications.Molecular biomedicine · 2025Review
- Article
- Benefits of Nutrients and Phytonutrients in Nuts and Legumes on Platelet Aggregation Through DNA Methylation.Molecular nutrition & food research · 2025Review
- Roles of Selected Bioactive Compounds in Inhibiting the Development and Progression of Cancer-A Review.International journal of molecular sciences · 2025Review
- Quercetin and hematological cancers: where are we and where are we going?Molecular biology reports · 2025Review
- Epi-nutrients for cancer prevention: Molecular mechanisms and emerging insights.Cell biology and toxicology · 2025Review
- Sea cucumber sulfated polysaccharides extract potentiates the anticancer effect of 5- fluorouracil on hepatocellular carcinoma cells.Scientific reports · 2025Article
- Article
- Traditional Chinese medicine for acute myelocytic leukemia therapy: exploiting epigenetic targets.Frontiers in pharmacology · 2024Review
- Phagocytosis-initiated tumor hybrid cells acquire a c-Myc-mediated quasi-polarization state for immunoevasion and distant dissemination.Nature communications · 2023Article
- Dietary polyphenols and their relationship to the modulation of non-communicable chronic diseases and epigenetic mechanisms: A mini-review.Food chemistry. Molecular sciences · 2023Article
- Phytochemicals and bioactive compounds effective against acute myeloid leukemia: A systematic review.Food science & nutrition · 2023Article
- Bioactive Phytoconstituents and Their Therapeutic Potentials in the Treatment of Haematological Cancers: A Review.Life (Basel, Switzerland) · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the present study, we investigated the molecular mechanisms underlying the pro-apoptotic effects of quercetin (Qu) by evaluating the effect of Qu treatment on DNA methylation and posttranslational histone modifications of genes related to the apoptosis pathway. This study was performed in vivo in two human xenograft acute myeloid leukemia (AML) models and in vitro using HL60 and U937 cell lines.
resultsQu treatment almost eliminates DNMT1 and DNMT3a expression, and this regulation was in part STAT-3 dependent. The treatment also downregulated class I HDACs. Furthermore, treatment of the cell lines with the proteasome inhibitor, MG132, together with Qu prevented degradation of class I HDACs compared to cells treated with Qu alone, indicating increased proteasome degradation of class I HDACS by Qu. Qu induced demethylation of the pro-apoptotic BCL2L11, DAPK1 genes, in a dose- and time-dependent manner. Moreover, Qu (50 μmol/L) treatment of cell lines for 48 h caused accumulation of acetylated histone 3 and histone 4, resulting in three- to ten fold increases in the promoter region of DAPK1, BCL2L11, BAX, APAF1, BNIP3, and BNIP3L. In addition, Qu treatment significantly increased the mRNA levels of all these genes, when compared to cells treated with vehicle only (control cells) (*p < 0.05).
conclusionsIn summary, our results showed that enhanced apoptosis, induced by Qu, might be caused in part by its DNA demethylating activity, by HDAC inhibition, and by the enrichment of H3ac and H4ac in the promoter regions of genes involved in the apoptosis pathway, leading to their transcription activation.
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