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Series GSE57498 Query DataSets for GSE57498
Status Public on Jun 04, 2014
Title Comparison of nucleosome occupancy and chromatin states between normal and cancer cell lines
Organism Homo sapiens
Experiment type Methylation profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary Background: Epigenetic modification is a hallmark of cancer cells achieved through altered patterns of DNA methylation, histone modifications and nucleosome positions. These events have only been described in detail at gene promoters. Results: Here, we integrate multiple epigenome-wide maps to evaluate the scope of global epigenetic reprogramming in cancer cells at enhancers and insulators. Using high-resolution simultaneous mapping of global DNA methylation and nucleosome positions within individual DNA strands (NOMe-Seq), we observe a reorganization of the DNA methylome coupled with simultaneous modulation of nucleosome depleted regions (NDRs) at distal regulatory elements in cancer cells. We show that while NDRs are preferentially found at enhancers in normal breast and prostate epithelial cells, there are fewer NDRs coupled with increased DNA methylation detected at enhancersin cancer cells. Our data suggests that the acquisition of a nucleosome is key to DNA hypermethylation susceptibility and contributes to epigenetic silencing of enhancers in cancer, which can notably occur without loss of H3K4me1. Further we observe that NDRs are not necessary for peripheral phasing of adjacent nucleosomes, contrary to the common dogma, and show that nucleosomes remain organized and phased, even in the absence of a NDR as an anchor. Finally we observe the potential for transcription factors (TF) to organize NDRs genome-wide; all TF-binding sites are strongly hypomethylated and some show extensive peripheral nucleosome phasing. Conclusion: Together our findings suggest that, in addition to epigenetic alterations to promoter regions in cancer, there is substantial disruption to the distal regulatory architecture that provides an additional layer of epigenetic plasticity in malignancy.
Overall design NOMe-seq, ChIP-seq for 5 marks and input control for breast normal (HMEC), breast cancer (MCF7), prostate normal (PrEC) and prostate cancer (PC3) cell lines
Contributor(s) Statham AL, Taberlay PC
Citation(s) 24916973
Submission date May 09, 2014
Last update date May 15, 2019
Contact name Aaron Statham
Organization name Garvan Institute of Medical Research
Department Cancer Department
Lab Epigenetics Research Laboratory
Street address 384 Victoria St
City Darlinghurst
State/province NSW
ZIP/Postal code 2010
Country Australia
Platforms (1)
GPL11154 Illumina HiSeq 2000 (Homo sapiens)
Samples (29)
GSM1383849 HMEC_NOMe-Seq
GSM1383850 MCF7_NOMe-Seq
GSM1383851 PrEC_NOMe-Seq
BioProject PRJNA246552
SRA SRP041828

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Supplementary file Size Download File type/resource
GSE57498_GCH.tsv.gz 956.5 Mb (ftp)(http) TSV
GSE57498_HMEC_ChromHMM.bed.gz 3.8 Mb (ftp)(http) BED
GSE57498_MCF7_ChromHMM.bed.gz 4.1 Mb (ftp)(http) BED
GSE57498_PC3_ChromHMM.bed.gz 2.9 Mb (ftp)(http) BED
GSE57498_PrEC_ChromHMM.bed.gz 3.5 Mb (ftp)(http) BED
GSE57498_RAW.tar 2.1 Mb (http)(custom) TAR (of BED)
GSE57498_WCG.tsv.gz 169.9 Mb (ftp)(http) TSV
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Raw data are available in SRA
Processed data are available on Series record

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