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Identification of DNA methylation-independent epigenetic events underlying clear cell renal cell carcinoma

ABSTRACT: Genome-wide analysis of endogenous and exogenous methylation in human ccRCC tumor and adjacent normal tissue to determine DNA methylation and chromatin structure states in ccRCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE70303 | GEO | 2016/03/15

SECONDARY ACCESSION(S): PRJNA288277

REPOSITORIES: GEO

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Identification of DNA methylation-independent epigenetic events underlying clear cell renal cell carcinoma

Project description:Genome-wide analysis of endogenous and exogenous methylation in human ccRCC tumor and adjacent normal tissue to determine DNA methylation and chromatin structure states in ccRCC. Nuclei from the 6 patient kidney tumor and normal samples were either treated or not-treated with M.SssI enzyme, DNA was extracted and bisulfite-converted, then hybridised to the Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482)

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Identification of DNA methylation-independent epigenetic events underlying clear cell renal cell carcinoma

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Project description:Alterations in chromatin accessibility independent of DNA methylation can affect cancer-related gene expression, but are often overlooked in conventional epigenomic profiling approaches. In this study, we describe a cost-effective and computationally simple assay called AcceSssIble to simultaneously interrogate DNA methylation and chromatin accessibility alterations in primary human clear cell renal cell carcinomas (ccRCC). Our study revealed significant perturbations to the ccRCC epigenome and identified gene expression changes that were specifically attributed to the chromatin accessibility status whether or not DNA methylation was involved. Compared with commonly mutated genes in ccRCC, such as the von Hippel-Lindau (VHL) tumor suppressor, the genes identified by AcceSssIble comprised distinct pathways and more frequently underwent epigenetic changes, suggesting that genetic and epigenetic alterations could be independent events in ccRCC. Specifically, we found unique DNA methylation-independent promoter accessibility alterations in pathways mimicking VHL deficiency. Overall, this study provides a novel approach for identifying new epigenetic-based therapeutic targets, previously undetectable by DNA methylation studies alone, that may complement current genetic-based treatment strategies. Cancer Res; 76(7); 1954-64. ©2016 AACR.

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