ArticleInternational journal of oncology2012
Green tea polyphenols increase p53 transcriptional activity and acetylation by suppressing class I histone deacetylases.
Article in International journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Pooled it
- An Overview of Targeting Some Cancer Hallmarks with Plant Polyphenols: A Step Toward Precision.Sub-cellular biochemistry · 2026Review
- Nano-phytochemical-based formulations as promising opportunities for prostate cancer therapy and management: a comprehensive narrative review.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Anticancer Plant Secondary Metabolites Induce Linker Histone Depletion from Chromatin.Frontiers in bioscience (Landmark edition) · 2024Article
- Dietary Polyphenols against Oxidative Stress in Head and Neck Cancer: What's New, What's Next.Journal of Cancer · 2024Review
- Dietary Plant Metabolites Induced Epigenetic Modification as a Novel Strategy for the Management of Prostate Cancer.Mini reviews in medicinal chemistry · 2024Review
- Phytocompounds targeting epigenetic modulations: an assessment in cancer.Frontiers in pharmacology · 2023Review
- Circulating (Poly)phenol Metabolites: Neuroprotection in a 3D Cell Model of Parkinson's Disease.Molecular nutrition & food research · 2022Article
- Niacin mitigates rumen epithelial damage in vivo by inhibiting rumen epithelial cell apoptosis on a high concentrate diet.Veterinary research communications · 2022Article
- Histone deacetylase inhibitors as a novel therapeutic approach for pheochromocytomas and paragangliomas.Oncology research · 2022Review
- Cardiac troponin I R193H mutant interacts with HDAC1 to repress phosphodiesterase 4D expression in cardiomyocytes.Genes & diseases · 2021Article
- The Major Constituent of Green Tea, Epigallocatechin-3-Gallate (EGCG), Inhibits the Growth of HPV18-Infected Keratinocytes by Stimulating Proteasomal Turnover of the E6 and E7 Oncoproteins.Pathogens (Basel, Switzerland) · 2021Article
- Role of Flavonoids as Epigenetic Modulators in Cancer Prevention and Therapy.Frontiers in genetics · 2021Review
- Targeting Epigenetic 'Readers' with Natural Compounds for Cancer Interception.Journal of cancer prevention · 2020Review
- Re-establishment of the epigenetic state and rescue of kinome deregulation in Ts65Dn mice upon treatment with green tea extract and environmental enrichment.Scientific reports · 2020Article
- Role of class I histone deacetylases in the regulation of maspin expression in prostate cancer.Molecular carcinogenesis · 2020Article
- Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer.Molecules (Basel, Switzerland) · 2020Review
- Review
- The interaction between gut microbiome and nutrients on development of human disease through epigenetic mechanisms.Genomics & informatics · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Acetylation of the tumor suppressor gene p53 at the carboxy-terminal lysine (Lys) residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis. Histone deacetylases (HDACs), a family of evolutionarily conserved enzymes, counterbalance the acetylation of lysine residues on histone and non-histone proteins. In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells. Treatment of cells with GTPs (2.5-10 µg/ml) and EGCG (5-20 µM) resulted in dose- and time-dependent inhibition of class I HDACs (HDAC1, 2, 3 and 8), albeit at varying levels. Discontinuation of treatment with GTP/EGCG resulted in the loss of p53 acetylation at both the sites in these cells. GTP/EGCG treatment also resulted in increased expression of p21/waf1 and Bax at the protein and message levels in these cells. The increased GTP/EGCG-mediated p53 acetylation enhanced its binding on the promoters of p21/waf1 and Bax, which was associated with increased accumulation of cells in the G0/G1 phase of the cell cycle and induction of apoptosis. Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53.
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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.