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Epigenetic regulation of Myc on retinoic acid receptor beta and PDLIM4 in RWPE1 cells
Author(s) -
He Meilan,
Vanaja Donkena Krishna,
Karnes R. Jeffrey,
Young Charles Y.F.
Publication year - 2009
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.21013
Subject(s) - epigenetics , dna methylation , cpg site , cancer research , dnmt3b , prostate cancer , epigenetic therapy , biology , methylation , methyltransferase , microbiology and biotechnology , retinoic acid , retinoic acid receptor , promoter , dna methyltransferase , prostate , cancer , cell culture , gene expression , genetics , gene
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‐2′‐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 69: 1643–1650, 2009. © 2009 Wiley‐Liss, Inc.