Devaney J M, Wang S, Furbert-Harris P, Apprey V, Ittmann M, Wang B-D, Olender J, Lee N H, Kwabi-Addo B
a Children's National Medical Center ; Center for Genetic Medicine Research ; Washington, DC USA.
Epigenetics. 2015;10(4):319-28. doi: 10.1080/15592294.2015.1022019. Epub 2015 Apr 11.
Increasing evidence suggests that aberrant DNA methylation changes may contribute to prostate cancer (PCa) ethnic disparity. To comprehensively identify DNA methylation alterations in PCa disparity, we used the Illumina 450K methylation platform to interrogate the methylation status of 485,577 CpG sites focusing on gene-associated regions of the human genome. Genomic DNA from African-American (AA; 7 normal and 3 cancers) and Caucasian (Cau; 8 normal and 3 cancers) was used in the analysis. Hierarchical clustering analysis identified probe-sets unique to AA and Cau samples, as well as common to both. We selected 25 promoter-associated novel CpG sites most differentially methylated by race (fold change > 1.5-fold; adjusted P < 0.05) and compared the β-value of these sites provided by the Illumina, Inc. array with quantitative methylation obtained by pyrosequencing in 7 prostate cell lines. We found very good concordance of the methylation levels between β-value and pyrosequencing. Gene expression analysis using qRT-PCR in a subset of 8 genes after treatment with 5-aza-2'-deoxycytidine and/or trichostatin showed up-regulation of gene expression in PCa cells. Quantitative analysis of 4 genes, SNRPN, SHANK2, MST1R, and ABCG5, in matched normal and PCa tissues derived from AA and Cau PCa patients demonstrated differential promoter methylation and concomitant differences in mRNA expression in prostate tissues from AA vs. Cau. Regression analysis in normal and PCa tissues as a function of race showed significantly higher methylation prevalence for SNRPN (P = 0.012), MST1R (P = 0.038), and ABCG5 (P < 0.0002) for AA vs. Cau samples. We selected the ABCG5 and SNRPN genes and verified their biological functions by Western blot analysis and siRNA gene knockout effects on cell proliferation and invasion in 4 PCa cell lines (2 AA and 2 Cau patients-derived lines). Knockdown of either ABCG5 or SNRPN resulted in a significant decrease in both invasion and proliferation in Cau PCa cell lines but we did not observe these remarkable loss-of-function effects in AA PCa cell lines. Our study demonstrates how differential genome-wide DNA methylation levels influence gene expression and biological functions in AA and Cau PCa.
越来越多的证据表明,异常的DNA甲基化变化可能导致前列腺癌(PCa)的种族差异。为了全面识别PCa差异中的DNA甲基化改变,我们使用Illumina 450K甲基化平台来检测485,577个CpG位点的甲基化状态,重点关注人类基因组的基因相关区域。分析中使用了非裔美国人(AA;7例正常样本和3例癌症样本)和白种人(Cau;8例正常样本和3例癌症样本)的基因组DNA。层次聚类分析确定了AA和Cau样本特有的探针集,以及两者共有的探针集。我们选择了25个与启动子相关的新型CpG位点,这些位点在种族间甲基化差异最大(倍数变化>1.5倍;校正P<0.05),并将Illumina公司阵列提供的这些位点的β值与7种前列腺癌细胞系中焦磷酸测序获得的定量甲基化进行比较。我们发现β值和焦磷酸测序之间的甲基化水平具有很好的一致性。在用5-氮杂-2'-脱氧胞苷和/或曲古抑菌素处理后,对8个基因的一个子集进行qRT-PCR基因表达分析,结果显示PCa细胞中基因表达上调。对来自AA和Cau PCa患者的匹配正常组织和PCa组织中的4个基因SNRPN、SHANK2、MST1R和ABCG5进行定量分析,结果表明AA与Cau前列腺组织中启动子甲基化存在差异,mRNA表达也随之不同。对正常组织和PCa组织进行种族回归分析,结果显示AA与Cau样本相比,SNRPN(P = 0.012)、MST1R(P = 0.038)和ABCG5(P < 0.0002)的甲基化发生率显著更高。我们选择了ABCG5和SNRPN基因,并通过蛋白质印迹分析以及siRNA基因敲除对4种PCa细胞系(2种来自AA患者,2种来自Cau患者)的细胞增殖和侵袭的影响来验证它们的生物学功能。敲低ABCG5或SNRPN均导致Cau PCa细胞系的侵袭和增殖显著降低,但在AA PCa细胞系中未观察到这些明显的功能丧失效应。我们的研究证明了全基因组DNA甲基化水平差异如何影响AA和Cau PCa中的基因表达和生物学功能。