Abstract
Prostate cancer is one of the most common non-cutaneous malignancies among men worldwide. Epigenetic aberrations, including changes in DNA methylation patterns and/or histone modifications, are key drivers of prostate carcinogenesis. These epigenetic defects might be due to deregulated function and/or expression of the epigenetic machinery, affecting the expression of several important genes. Remarkably, epigenetic modifications are reversible and numerous compounds that target the epigenetic enzymes and regulatory proteins were reported to be effective in cancer growth control. In fact, some of these drugs are already being tested in clinical trials. This review discusses the most important epigenetic alterations in prostate cancer, highlighting the role of epigenetic modulating compounds in pre-clinical and clinical trials as potential therapeutic agents for prostate cancer management.
Highlights
Prostate cancer Prostate cancer (PCa) is one of the most common malignancies worldwide and a leading cause of cancer-related morbidity and mortality [1]
GSK126 combined with conventional chemotherapy sensitized castration-resistant prostate cancer (CRPC) cells to apoptosis and growth inhibition both in vitro and in vivo [251]. These results suggest that enhancer of zeste homolog 2 (EZH2) inhibitors might be helpful to increase CRPC patient response to conventional therapy
PCa cells exposed to vorinostat/SAHA combined with olaparib demonstrated a synergistic decrease in cell viability and clonogenicity, as well as an increase in apoptosis and DNA damage compared with single agent, not affecting normal prostate cells [262]
Summary
Prostate cancer Prostate cancer (PCa) is one of the most common malignancies worldwide and a leading cause of cancer-related morbidity and mortality [1]. Pre-clinical activity of DNMT inhibitors in prostate cancer In a pre-clinical assay, PCa cells chronically exposed to 5-aza-2′-deoxycytidine for 21 days, exhibited a marked decrease in tumor cell proliferation and AR reactivation, with concomitantly increased PSA protein levels. This compound repressed DNMT activity and expression, reducing global DNA methylation in androgen-responsive PCa cells.
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