Unknown,Transcriptomics,Genomics,Proteomics

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Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma [ChIP-seq]

ABSTRACT: ChIP-Seq analysis of a pediatric human diffuse intrinsic pontine glioma (DIPG) cell line SF8628, harboring the K27M mutation. Goal was to obtain quantitative estimates of K27me3 immunoprecipitation change between vehicle-treated SF8628 cells [dimethyl sulfoxide, (DMSO)] and SF8628 cells incubated with 6 mM GSKJ4 at 24 hours and 72 hours. Three-condition experiment: 72 h GSKJ4-treated cells vs. 24 h GSKJ4-treated cells vs. DMSO-treated cells. Biological replicates: 1 cell line, each with 2 technical replicates per condition.

ORGANISM(S): Homo sapiens

SUBMITTER: Rintaro Hashizume

PROVIDER: E-GEOD-59496 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Alcohol is a major risk factor for hepatocellular carcinoma (HCC) although the mechanisms underlying the alcohol-related liver carcinogenesis are still poorly understood. Alcohol is known to increase hepatocarcinogenesis possibly by inducing aberrant DNA methylation through the reduced provision of methyl groups within the hepatic one-carbon metabolism. Whether the epigenetically-regulated pathways in alcohol-associated HCC can be reversible or modifiable by nutritional factors is unknown. The aim of the present study was to investigate the genome wide promoter DNA methylation profiles along with array-based, gene expression profiles in non-viral, alcohol-associated HCC. From eight HCC patients the methylation status and transcriptional levels of all annotated genes were compared by analyzing HCC tissue and the cancer-free surrounding liver tissue, following curative surgery. After merging both the DNA methylation and gene expression data, we identified 159 hypermethylated-repressed, 30 hypomethylated-induced, 49 hypermethylated-induced and 56 hypomethylated-repressed genes. A number of potentially novel candidate tumor-suppressor genes (FAM107A, IGFALS, MT1G, MT1H, RNF180) demonstrated promoter hypermethylation and transcriptional repression in alcohol-associated HCC. Notably, promoter DNA methylation appeared as the regulatory mechanism for the transcriptional repression of genes controlling the retinol metabolic pathway (ADH1A, ADH1B, ADH6, CYP3A43, CYP4A22, RDH16) and SHMT1, a key gene within one-carbon metabolism. A genome-wide DNA methylation approach linked up with array-based gene expression profiles allowed identifying a number of novel, epigenetically-regulated candidate tumor-suppressor genes in alcohol-associated hepatocarcinogenesis. Retinol metabolism genes and SHMT1 are also epigenetically-regulated through promoter DNA methylation in alcohol-associated hepatocarcinogenesis. 16 samples (8 control samples from non-neoplastic liver tissue, 8 test samples from hepatocellular carcinoma) from 8 patients affected from hepatocellular carcinoma were analyzed.

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Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma [ChIP-seq]

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