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Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [CUT&RUN]

ABSTRACT: Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [CUT&RUN]

PROVIDER: PRJNA996581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25345302_1.fastq.gz	Fastqsanger.gz
	SRR25345302_2.fastq.gz	Fastqsanger.gz
	SRR25345303_1.fastq.gz	Fastqsanger.gz
	SRR25345303_2.fastq.gz	Fastqsanger.gz
	SRR25345304_1.fastq.gz	Fastqsanger.gz

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Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [CUT&RUN]

Project description:Here we investigate the impact of epigenetic therapy with Decitabine in endocrine-resistant ER+ breast cancer by using patient-derived xenograft (PDX) models. Decitabine treatment restrained tumour growth, inhibited cell proliferation and resulted in significant loss of DNA methylation, particularly at enhancers and repetitive elements. Systematic integration of matched in situ Hi-C / PCHi-C, EPIC, RNA-seq and ChIP–seq datasets revealed widespread differences in epigenome regulation and enhancer-promoter communication with Decitabine. We find that loss of DNA methylation with Decitabine strongly affects the open (A) and closed (B) compartment structure and TAD boundary insulation. Our study identified and focused on key DNA methylation-dependent, enhancer ER binding sites that are activated in Decitabine-treated PDX tumours, enabling direct interactions between promoters and multiple distal enhancers, inducing expression of ER target genes and pathways. Overall, we demonstrate that epigenetic therapy inhibits tumour progression through to rewiring of ER-mediated 3D chromatin interactions and transcriptome programs. Our findings suggest that targeting the 3D epigenome with epigenetic therapies represents a promising strategy for anti-cancer treatment in ER+ endocrine resistant breast cancer patients.

2023-07-24 | GSE237769 | GEO

Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [WGBS]

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Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [WGBS]

Project description:Epigenetic therapy targets the 3D epigenome in endocrine-resistant breast cancer [WGBS]

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Cut-and-Run in situ factor profiling maps DNA binding and 3D contact sites at high resolution

Project description:Unlike Chromatin Immunoprecipitation (ChIP), which fragments and solubilizes total chromatin, Cut-and-Run is performed in situ, allowing for both high-resolution chromatin mapping and probing of the local chromatin environment. When applied to yeast and human nuclei, Cut-and-Run yielded precise transcription factor profiles while avoiding cross-linking and solubilization issues. Cut-and-Run is simple to perform and at low temperatures is inherently robust, with extremely low backgrounds that make it especially cost-effective for transcription factor and chromatin profiling. When used in conjunction with native ChIP-seq and applied to human CTCF, Cut-and-Run mapped high-resolution 3D directional interactions. We conclude that Cut- and-Run is a suitable complement or replacement for ChIP-seq that can also provide 3D mapping information.

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Deregulation of the three-dimensional epigenome in endocrine resistant breast cancer

Project description:Around 35% of Estrogen Receptor (ER) positive patients develop resistance and relapse, highlighting the need to further understand the mechanisms underpinning endocrine resistance in breast cancer. Here, we study 3-dimensional (3D) epigenome remodelling in endocrine resistant breast cancer cells. We show that chromatin interactions both within and between topologically associating domains (TADs) frequently change in resistant breast cancer cells and that alterations in active (A-type) and inactive (B-type) chromosomal compartments are associated with decreased ER binding and atypical interactions and gene expression. Finally, we identify differentially interacting ER-bound regions that preferentially connect active enhancers and promoters associated with altered expression of ER-regulated genes. Importantly, interactions specifically associated with endocrine resistance, often occur coincidently with hypermethylation of ER binding. Our results demonstrate that 3D epigenome remodelling is a key mechanism of endocrine resistance that consists of differential chromatin interactions and aberrant DNA methylation at ER-regulated enhancer regions.

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The potential of epigenetic therapy to target the 3D epigenome in endocrine-resistant breast cancer

Project description:The potential of epigenetic therapy to target the 3D epigenome in endocrine-resistant breast cancer

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Epigenetic reprogramming at estrogen-receptor binding sites alters the 3D chromatin landscape in endocrine resistant breast cancer [WGS]

Project description:Endocrine therapy resistance invariably develops in estrogen receptor positive (ER+) breast cancer, but the underlying molecular mechanisms are largely unknown. Here, we show that 3-dimensional (3D) chromatin interactions both within and between topologically associating domains (TADs) frequently change in ER+ endocrine resistant breast cancer cells and that the differential interactions are enriched for genetic variants at CTCF-bound anchors. Ectopic chromatin interactions are preferentially enriched at active enhancers and promoters and ER binding sites and are associated with altered expression of ER-regulated genes, consistent with dynamic remodelling of ER pathways accompanying the development of endocrine resistance. Importantly, new 3D chromatin interactions often occur coincidently with hypermethylation and loss of ER binding. Additionally, alterations in active (A-type) and inactive (B-type) chromosomal compartments are also associated with decreased ER binding and atypical interactions and gene expression. Together, our results suggest that 3D epigenome remodelling is a key mechanism underlying endocrine resistance in ER+ breast cancer.

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Epigenetic reprogramming at estrogen-receptor binding sites alters the 3D chromatin landscape in endocrine resistant breast cancer [WGBS]

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Metabolic regulation of the epigenome drives lethal infantile ependymoma [Cut&Run]

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