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- W2896075290 abstract "Aberrant DNA methylation is commonly observed in cancer genomes, including focal gene promoter hypermethylation and global hypomethylation. While the gain of this repressive epigenetic modification at gene promoter has been relatively well studied, global loss of DNA methylation in cancer cells remains poorly understood. As previously reported, the loss of DNA methylation results in the formation of partially methylated domains (PMDs), large genomic segments with reduced DNA methylation. Intriguingly, genes residing in PMDs show little to no transcriptional change, potentially compensated by the histone H3 lysine 9 tri-methylation (H3K9me3) and histone H3 lysine 27 tri-methylation (H3K27me3) repressive histone modifications. We have observed that large PMDs are typically enriched with both of these repressive epigenetic marks in a particular pattern. Therefore, we hypothesize that occupancy of H3K27me3 at the boundaries might act as a barrier in demarcating PMDs. Using A375, a melanoma cell line, as a model, we employed techniques to analyze the epigenome including whole genome bisulfite sequencing (MethylC-seq) and chromatin immunoprecipitation sequencing (ChIP-seq). Furthermore, we utilized several approaches to engineer either the genomic sequence or epigenomic marks at PMDs boundaries and studied their effects on other epigenetic marks. This study aims to elucidate the interplay between distinct epigenetic modifications." @default.
- W2896075290 created "2018-10-26" @default.
- W2896075290 creator A5080055959 @default.
- W2896075290 date "2018-05-31" @default.
- W2896075290 modified "2023-09-26" @default.
- W2896075290 title "Delineating interplay between epigenetic pathways" @default.
- W2896075290 doi "https://doi.org/10.14711/thesis-991012586766703412" @default.
- W2896075290 hasPublicationYear "2018" @default.
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