Epigenetic modifications and gene expression regulation in testosterone-mediated prostate cancer: A systematic review

Background Prostate cancer is known to be caused by the androgen receptor (AR) axis and testosterone, emerging evidence highlights the significance of epigenetic modifications in mediating androgen-dependent tumorigenesis and therapy resistance. Methodology The literature search was conducted in Scopus, PubMed, and Google Scholar following PRISMA guidelines. Case-control, clinical and preclinical studies, and human clinical trials analyzed epigenetic modifications in testosterone-mediated prostate cancer were included. Studies that did not analyze epigenetic alterations in prostate cancer or focused on other cancer types were excluded. Result Prostate cancer is largely caused by DNA methylation, which controls gene expression. Genes are silenced when CpG islands are hypermethylated, and genomic instability is exacerbated by hypomethylation. Emerging therapeutic strategies, such as DNMT inhibitors and combination therapies with AR pathway inhibitors, are being explored to target aberrant DNA methylation in prostate cancer treatment. Prostate cancer development and androgen receptor signaling are influenced by chromatin remodeling and gene regulation, both of which are significantly impacted by histone changes. Conclusion Epigenetic dysregulation drives prostate cancer progression by silencing tumor suppressors, activating oncogenes, and promoting therapy resistance. These changes have potential as therapeutic targets for better patient clinical care.