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Homo sapiens

ABSTRACT: Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [RNA-seq]

PROVIDER: PRJNA390528 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5683170_1.fastq.gz	Fastqsanger.gz
	SRR5683170_2.fastq.gz	Fastqsanger.gz
	SRR5683171_1.fastq.gz	Fastqsanger.gz
	SRR5683171_2.fastq.gz	Fastqsanger.gz
	SRR5683172_1.fastq.gz	Fastqsanger.gz

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Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors

Project description:Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors

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Project description:Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [EPIC methylation]

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Project description:Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [EPIC methylation 2]

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Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [EPIC methylation 2]

Project description:Aberrant promoter DNA hypermethylation is a hallmark of cancer; however, whether this is sufficient to drive cellular transformation in the absence of genetic mutations is not clear. To investigate this question, we use a CRISPR/dCas9 based epigenetic editing tool, where an inactive form of Cas9 is fused to DNMT3A and its regulator DNMT3L. Using this system, we show simultaneous de novo DNA methylation of genes commonly methylated in cancer, CDKN2A, RASSF1, HIC1 and PTEN in primary myoepithelial cells isolated from healthy human breast tissue. We find that promoter methylation is maintained in this system, even in the absence of the fusion construct and results in sustained repression of CDKN2A and RASSF1 transcripts which prevents cells from entering senescence. The phenotype is associated with retuned expression of a subset of genes to levels in early passage cells; however, the outgrowing myoepithelial cells are not immortal but proliferate for 25-30 population doublings before cell cycle arrest. Finally, we show that the key driver of this phenotype is repression of CDKN2A transcript p16, but prolonged proliferation is enhanced by combined hypermethylation and repression of both CDKN2A transcripts p16 and p14. This work demonstrates that hit-and-run epigenetic events can prevent senescence entry, a potential first step in the disease process.

2017-08-07 | GSE100208 | GEO

Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [EPIC methylation]

2017-08-07 | GSE100184 | GEO

Hit-and-run epigenetic editing prevents senescence entry in primary breast cells from healthy donors [RNA-seq]

Project description:Aberrant promoter DNA hypermethylation is a hallmark of cancer; however, whether this is sufficient to drive cellular transformation in the absence of genetic mutations is not clear. To investigate this question, we use a CRISPR/dCas9 based epigenetic editing tool, where an inactive form of Cas9 is fused to DNMT3A and its regulator DNMT3L. Using this system, we show simultaneous de novo DNA methylation of genes commonly methylated in cancer, CDKN2A, RASSF1, HIC1 and PTEN in primary myoepithelial cells isolated from healthy human breast tissue. We find that promoter methylation is maintained in this system, even in the absence of the fusion construct and results in sustained repression of CDKN2A and RASSF1 transcripts which prevents cells from entering senescence. The phenotype is associated with retuned expression of a subset of genes to levels in early passage cells; however, the outgrowing myoepithelial cells are not immortal but proliferate for 18-20 population doublings before cell cycle arrest. Finally, we show that the key driver of this phenotype is repression of CDKN2A transcript p16, but prolonged proliferation is enhanced by combined hypermethylation and repression of both CDKN2A transcripts p16 and p14. This work demonstrates that hit-and-run epigenetic events can prevent senescence entry, a potential first step in the disease process.

2017-08-07 | GSE100027 | GEO

Homo sapiens

Project description:Inheritable Silencing of Endogenous Genes by Hit-and-Run Targeted Epigenetic Editing

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CUT&RUN-seq of H3K9me3, H4K20me3 or H3K4me3 in mESC after epigenetic editing and upon release of the trigger

Project description:Enrichment of histone marks was assessed by CUT&RUN-sequencing after epigenetic editing with dCas9::KRAB (or dCas9::GFP as a control) and subsequently upon release of the trigger. Samples were collected after 7 days of DOX induction (epigenetic editing) and after 4 and 7 days of DOX washout (release of the trigger).

2021-11-23 | E-MTAB-10525 | biostudies-arrayexpress

Single-cell RNA sequencing of human nasal swab from healthy donors

Project description:Understanding on pathogenesis of COVID-19 is rapidly growing, but primary target cells of SARS-CoV-2 infection is still not known. Here, we performed single cell RNA sequencing on human nasal swab from healthy donors to investigate the expression patterns of host cell entry factors of SARS-CoV-2.

2021-04-06 | GSE171488 | GEO

Hit-and-run silencing of endogenous DUX4 by targeting DNA hypomethylation on D4Z4 repeats in facioscapulohumeral muscular dystrophy [RNA-seq]

Project description:Facioscapulohumeral muscular dystrophy (FSHD), a progressive skeletal muscle disorder, is epigenetically characterized with DNA hypomethylation of D4Z4 repeats in 4q35 region, allowing aberrant DUX4 expression. Sustainable DUX4 suppression is a promising therapeutic clue to prevent disease progression, but most of the supposed methods depend on expression of their mediator biochemical entity, potentially narrowing QoL of individuals with FSHD in the clinical context. In this study, we report that by applying hit-and-run silencing with dCas9-mediated epigenetic editing targeting DNA hypomethylation on D4Z4 repeats, we could achieve suppression of endogenous DUX4 in our FSHD patients-derived iPSC model. Notably, DNA methylation was significantly upregulated in FSHD cells and suppression effect was observed at least two weeks after intervention, which was not the case by transient treatment of typical dCas9-KRAB alone. Off-target analysis showed that despite the potential genome-wide risk in DNA methylation, the impact on transcriptome was limited. We propose that hit-and-run silencing can be a promising option to prevent disease progression with minimum intervention for individuals with FSHD, motivating further study for clinical development.

2024-03-31 | GSE201178 | GEO

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