ArticleCancer2010
Genistein reverses hypermethylation and induces active histone modifications in tumor suppressor gene B-Cell translocation gene 3 in prostate cancer.
Article in Cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 178 citations in OpenAlex.
- Effects of genistein supplementation on genome‑wide DNA methylation and gene expression in patients with localized prostate cancer.International journal of oncology · 2017Trial
- Trial
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- Investigating the Epigenetic Therapeutic Potential of Natural Compounds in Cancer.International journal of molecular sciences · 2025Review
- Oxidative-Inflammatory Crosstalk and Multi-Target Natural Agents: Decoding Diabetic Vascular Complications.Current issues in molecular biology · 2025Review
- Epi-nutrients for cancer prevention: Molecular mechanisms and emerging insights.Cell biology and toxicology · 2025Review
- BTG3-dependent VCP/p97 nuclear translocation is required for efficient repair of UV-induced DNA lesions.Nucleic acids research · 2025Article
- Epigenetic and biogenetic regulation by polyphenols in prostate cancer in the context of 3P medicine.The EPMA journal · 2025Review
- Opportunities and challenges of foodborne polyphenols applied to anti-aging health foods.Food science and biotechnology · 2024Review
- A keratinocyte-adipocyte signaling loop is reprogrammed by loss of BTG3 to augment skin carcinogenesis.Cell death and differentiation · 2024Article
- The Pros and Cons of Estrogens in Prostate Cancer: An Update with a Focus on Phytoestrogens.Biomedicines · 2024Review
- Recent Advancements in Research on DNA Methylation and Testicular Germ Cell Tumors: Unveiling the Intricate Relationship.Biomedicines · 2024Review
- A Computational Approach for the Discovery of Novel DNA Methyltransferase Inhibitors.Current issues in molecular biology · 2024Article
- The Use of Soy Isoflavones in the Treatment of Prostate Cancer: A Focus on the Cellular Effects.Nutrients · 2023Review
- Inhibition of Cancer Development by Natural Plant Polyphenols: Molecular Mechanisms.International journal of molecular sciences · 2023Review
- Regulation of Host Defense Peptide Synthesis by Polyphenols.Antibiotics (Basel, Switzerland) · 2023Review
- Methyl Group Metabolism in Differentiation, Aging, and Cancer.International journal of molecular sciences · 2022Review
- Natural Bioactive Compounds Targeting Histone Deacetylases in Human Cancers: Recent Updates.Molecules (Basel, Switzerland) · 2022Review
31 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
background: B-cell translocation gene 3 (BTG3/ANA/APRO4) is a candidate tumor suppressor gene in some malignancies. We report here that B-cell translocation gene 3 (BTG3) is transcriptionally down-regulated in prostate cancer and the mechanism of inactivation is through promoter hypermethylation.
methods: Prostate cancer and normal cell lines were treated with different doses of genistein and 5-aza-2'-deoxycytidine (5Aza-C). BTG3 messenger ribonucleic acid (mRNA) expression was determined by quantitative real-time polymerase chain reaction in tissues and cell lines. Bisulfate-modified polymerase chain reaction, cloning and sequencing were used to examine promoter methylation in tumor samples and cell lines. Enzyme activity/inhibition assays were done to check the effect of genistein and 5Aza-C on DNA methyltransferases. ChIP assay was performed to analyze chromatin modifications caused by genistein treatment.
results: BTG3 mRNA expression was down-regulated in cancer tissues and cells. Genistein and 5Aza-C induced BTG3 mRNA expression in all PC cell lines. Complete methylation of BTG3 promoter in tumor samples and cancer cell lines was observed. Genistein and 5Aza-C treatment significantly decreased promoter methylation, reactivating BTG3 expression. Genistein and 5Aza-C increased levels of acetylated histones 3, 4, histone 3 dimethylated at lysine 4, histone 3 trimethylated at lysine 4, and RNA polymerase II, decreased DNA methyl transferase and methyl-binding domain protein 2 activity, and increased histone acetyl transferase (HAT) activity.
conclusions: This is the first report to show that BTG3 is silenced in prostate cancer and can be reactivated by genistein-induced promoter demethylation and active histone modification. Genistein showed similar effects to that of 5Aza-C, which is currently undergoing phase 2 clinical trials as a treatment for prostate cancer. Because genistein is a natural, nontoxic, and dietary isoflavone, these results indicate that genistein is a novel, advantageous therapeutic agent for treating prostate cancer.
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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.