ArticleBMC cancer2012
Genistein cooperates with the histone deacetylase inhibitor vorinostat to induce cell death in prostate cancer cells.
Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- The paradox of cellular senescence in prostate cancer: from tumor suppression to tumor promotion.Frontiers in oncology · 2026Review
- Review
- Increasing Life Expectancy with Plant Polyphenols: Lessons from the Mediterranean and Japanese Diets.Molecules (Basel, Switzerland) · 2025Review
- Cellular and Molecular Mechanisms Modulated by Genistein in Cancer.International journal of molecular sciences · 2025Review
- Genistein as a Chemo-modulatory Agent: Exploring its Potential in Chemosensitization and Combinatorial Therapeutic Strategies for Cancer Treatment.Current topics in medicinal chemistry · 2025Review
- Stochasticity of anticancer mechanisms underlying clinical effectiveness of vorinostat.Heliyon · 2024Review
- Unveiling the Molecular Landscape ofInternational journal of molecular sciences · 2023Article
- Targeting Histone Deacetylases: Opportunities for Cancer Treatment and Chemoprevention.Pharmaceutics · 2022Review
- Neuromodulating roles of estrogen and phytoestrogens in cognitive therapeutics through epigenetic modifications during aging.Frontiers in aging neuroscience · 2022Review
- A Mini-Review of Flavone Isomers Apigenin and Genistein in Prostate Cancer Treatment.Frontiers in pharmacology · 2022Review
- Dietary Phytoestrogens and Their Metabolites as Epigenetic Modulators with Impact on Human Health.Antioxidants (Basel, Switzerland) · 2021Review
- Genistein-induced Anticancer Effects on Acute Leukemia Cells Involve the Regulation of Wnt Signaling Pathway Through H4K20me1 Rather Than DNA Demethylation.Current medical science · 2021Article
- Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021Review
- Epigenetic alterations and genetic variations of angiotensin-converting enzyme 2 (ACE2) as a functional receptor for SARS-CoV-2: potential clinical implications.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Review
- Genistein: An Integrative Overview of Its Mode of Action, Pharmacological Properties, and Health Benefits.Oxidative medicine and cellular longevity · 2021Review
- Studies of hormonal regulation, phenotype plasticity, bone metastasis, and experimental therapeutics in androgen-repressed human prostate cancer (ARCaP) model.American journal of clinical and experimental urology · 2021Review
- EMT transcription factor ZEB1 alters the epigenetic landscape of colorectal cancer cells.Cell death & disease · 2020Article
- Recent progress on the effects of microRNAs and natural products on tumor epithelial-mesenchymal transition.OncoTargets and therapy · 2017Review
- Histone and Non-Histone Targets of Dietary Deacetylase Inhibitors.Current topics in medicinal chemistry · 2016Review
- Epigenetic and miRNAs Dysregulation in Prostate Cancer: The role of Nutraceuticals.Anti-cancer agents in medicinal chemistry · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAmong American men, prostate cancer is the most common, non-cutaneous malignancy that accounted for an estimated 241,000 new cases and 34,000 deaths in 2011. Previous studies have suggested that Wnt pathway inhibitory genes are silenced by CpG hypermethylation, and other studies have suggested that genistein can demethylate hypermethylated DNA. Genistein is a soy isoflavone with diverse effects on cellular proliferation, survival, and gene expression that suggest it could be a potential therapeutic agent for prostate cancer. We undertook the present study to investigate the effects of genistein on the epigenome of prostate cancer cells and to discover novel combination approaches of other compounds with genistein that might be of translational utility. Here, we have investigated the effects of genistein on several prostate cancer cell lines, including the ARCaP-E/ARCaP-M model of the epithelial to mesenchymal transition (EMT), to analyze effects on their epigenetic state. In addition, we investigated the effects of combined treatment of genistein with the histone deacetylase inhibitor vorinostat on survival in prostate cancer cells.
methodsUsing whole genome expression profiling and whole genome methylation profiling, we have determined the genome-wide differences in genetic and epigenetic responses to genistein in prostate cancer cells before and after undergoing the EMT. Also, cells were treated with genistein, vorinostat, and combination treatment, where cell death and cell proliferation was determined.
resultsContrary to earlier reports, genistein did not have an effect on CpG methylation at 20 μM, but it did affect histone H3K9 acetylation and induced increased expression of histone acetyltransferase 1 (HAT1). In addition, genistein also had differential effects on survival and cooperated with the histone deacteylase inhibitor vorinostat to induce cell death and inhibit proliferation.
conclusionOur results suggest that there are a number of pathways that are affected with genistein and vorinostat treatment such as Wnt, TNF, G2/M DNA damage checkpoint, and androgen signaling pathways. In addition, genistein cooperates with vorinostat to induce cell death in prostate cancer cell lines with a greater effect on early stage prostate 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.