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Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations [ChIP-seq]

ABSTRACT: A three-dimensional chromatin state underpins the structural and functional basis of the genome by bringing regulatory elements and genes into close spatial proximity to ensure proper, cell-type specific gene expression profiles. Here, we perform HiC chromosome conformation, ChIP-seq and RNA-seq to investigate how the three-dimensional organization of the cancer genome is disrupted in the context of epigenetic remodelling and atypical gene expression programs. Hi-C, ChIP-seq and RNA-seq were conducted in three human prostate cell lines: normal prostate epithelial cells (PrEC) and prostate cancer cells (PC3 and LNCaP).

ORGANISM(S): Homo sapiens

SUBMITTER: Joanna Achinger-Kawecka

PROVIDER: E-GEOD-73783 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations [RNA-seq]

Project description:A three-dimensional chromatin state underpins the structural and functional basis of the genome by bringing regulatory elements and genes into close spatial proximity to ensure proper, cell-type specific gene expression profiles. Here, we perform HiC chromosome conformation, ChIP-seq and RNA-seq to investigate how the three-dimensional organization of the cancer genome is disrupted in the context of epigenetic remodelling and atypical gene expression programs. Hi-C, ChIP-seq and RNA-seq were conducted in three human prostate cell lines: normal prostate epithelial cells (PrEC) and prostate cancer cells (PC3 and LNCaP).

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Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations [RNA-seq]

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Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations [ChIP-seq]

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Three-dimensional disorganisation of the cancer genome occurs coincident with long range genetic and epigenetic alterations

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Comparison of nucleosome occupancy and chromatin states between normal and cancer cell lines

Project description: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. 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

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