Unknown,Transcriptomics,Genomics,Proteomics

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MeDIP-Chip of PrEC, LnCAP, and PC3 cells treated with vehicle control, sulforaphane, or 3,3’-diindolylmethane

ABSTRACT: Effects of sulforaphane and 3,3’-diindolylmethane on genome-wide promoter methylation in normal prostate epithelial cells and prostate cancer cells This study was undertaken to determine the genome-wide effects of sulforaphane (SFN) and 3,3’-diindolylmethane (DIM) on promoter methylation in normal prostate epithelial cells and prostate cancer cells. Nimblegen Human DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Array was used in this study. We hypothesize that both SFN and DIM are effective dietary modulators of DNA methylation due to their inhibitory effects on DNMT expression, and that SFN and DIM can differentially affect the promoter methylation profiles in normal and cancerous prostate epithelial cells. Normal prostate epithelial cells (PrEC), androgen-dependent prostate cancer epithelial cells (LnCAP) and androgen-independent prostate cancer epithelial cells (PC3) were treated with vehicle control, 15uM SFN, or 15uM DIM for 48h in triplicates

ORGANISM(S): Homo sapiens

SUBMITTER: Carmen Wong

PROVIDER: E-GEOD-47017 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Beginning with precursor lesions, aberrant DNA methylation marks the entire spectrum of prostate cancer progression. We mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). A Hidden Markov Model (HMM)-based algorithm previously used for Chip-Seq data analysis(http://www.sph.umich.edu/csg/qin/HPeak) was used to locate peaks from mapped reads obtained in each sequencing run. The total methylation events in intergenic/intronic regions between benign adjacent and cancer tissues were comparable. While approximately 20% of all CpG islands (CGIs) (68,508) were methylated in tissues, promoter CGI methylation gradually increased from ~12.6% in benign samples to 19.3% and 21.8% in localized and metastatic cancer tissues. We found distinct patterns in promoter methylation around transcription start sites, where methylation occurred directly on the CGIs, flanking regions and on CGI sparse promoters. Among the 6,691 methylated promoters in prostate tissues, 2481 differentially methylated regions (DMRs) are cancer specific and several previously studied targets were among them. A novel cancer specific DMR in WFDC2 promoter showed 77% methylation in cancer (17/22), 100% methylation in transformed prostate cell lines (6/6), none in the benign tissues (0/10) and normal PrEC cells. Integration of LNCaP DNA methylation and H3K4me3 data suggested a role for DNA methylation in alternate transcription start site utilization. While methylated promoters containing CGIs had mutually exclusive H3K4me3 modification, the histone mark was absent in CGI sparse promoters. Finally, we observed difference in methylation of LINE-1 elements between transcription factor ERG positive and negative cancers. The comprehensive methylome map presented here will further our understanding of epigenetic regulation of the prostate cancer genome. We mapped the global DNA methylation patterns in prostate tissues (n=17; data not available in GEO - being deposited in dbGaP for controlled access) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). For replicate analysis in cell lines, a total of 4 runs were completed for PrEC prostate normal cell line, and 5 runs were completed for LNCaP prostate cancer cell line. For tissue samples, 2 benign prostate samples were ran twice on illumina next generation sequencing platform to access overall repeatability of M-NGS.

Dataset Information

MeDIP-Chip of PrEC, LnCAP, and PC3 cells treated with vehicle control, sulforaphane, or 3,3’-diindolylmethane

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