BACKGROUND. Hypermethylation of CpG islands is a common epigenetic alteration associated with cancer. Tumor suppressor genes retinoic acid receptor beta (RARβ) and PDLIM4 are hypermethylated and silenced in prostate cancer (PCa) tissues and PCa cell lines compared to normal prostate cells. METHODS. In this study, a benign prostate epithelial cell line RWPE1 was used as a model to study the epigenetic regulation of Myc on the RARβ and PDLIM4 promoters. Forced Myc overexpression inhibited the RARβ and PDLIM4 expression. RESULTS. Pyrosequencing study showed that Myc overexpression increased methylation in several CpG sites of both promoters. A DNA methylation inhibitor 5-aza-20-deoxycytidine reversed the epigenetic alteration effect of Myc on both RARβ and PDLIM4. CONCLUSION. The epigenetic regulation of Myc may be related to its up-regulation of the DNA methyltransferase DNMT3a and DNMT3b.
- Prostate cancer
ASJC Scopus subject areas