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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiC]

ABSTRACT: The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiC]

PROVIDER: PRJNA1001888 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25506308_1.fastq.gz	Fastqsanger.gz
	SRR25506308_2.fastq.gz	Fastqsanger.gz
	SRR25506309_1.fastq.gz	Fastqsanger.gz
	SRR25506309_2.fastq.gz	Fastqsanger.gz
	SRR25506310_1.fastq.gz	Fastqsanger.gz

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiC]

Project description:Epstein-Barr virus (EBV) establishes lifelong asymptomatic infection by replication of its chromatinized episomes with the host genome. EBV exhibits different latency-associated transcriptional repertoires, each with distinct three-dimensional structures. CTCF, Cohesin and PARP1 are involved in maintaining viral latency and establishing episome architecture. Epstein-Barr virus-associated gastric cancer (EBVaGC) represents 1.3% to 30.9% of all gastric cancers globally. EBV-positive gastric cancers exhibit an intermediate viral transcription profile known as "Latency II", expressing specific viral genes and noncoding RNAs. In this study, we investigated the impact of PARP1 inhibition on CTCF/Cohesin binding in Type II latency. We observed destabilization of the binding of both factors, leading to a disrupted three-dimensional architecture of the episomes and an altered viral gene expression. Despite sharing the same CTCF binding profile, Type I, II, and III latencies exhibit different 3D structures that correlate with variations in viral gene expression. Additionally, our analysis of H3K27ac-enriched interactions revealed differences between Type II latency episomes and a link to cellular transformation through docking of the EBV genome at specific sites of the Human genome, thus promoting oncogene expression. Overall, this work provides insights into the role of PARP1 in maintaining active latency and novel mechanisms of EBV-induced cellular transformation.

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC

Project description:The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiChIP]

Project description:The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiChIP]

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [HiChIP]

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [RNA-seq]

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [ChIP-seq]

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [RNA-seq]

Project description:The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [RNA-seq]

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The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [ChIP-seq]

Project description:The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC [ChIP-seq]

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Effect of knockdown of miR-BART19-3p on gene expression of AGS EBV cells

Project description:EBV microRNAs, especially rightward transcript (BART) microRNAs play key roles in the tumor growth of EBVaGC. However, the effects of EBV-miR-BART19-3p in EBVaGC remain largely unknown. Here, we report that EBV-miR-BART19-3p is highly expressed in EBVaGC and promoted the proliferation of EBV-associated gastric cancer cells in vitro and accelerate xenograft tumor growth in vivo. Molecularly, EBV-miR-BART19-3p directly targets the growth arrest and DNA damage-inducing protein Beta mRNA (GADD45B) and downregulates its protein expression, which consequently reduce cell cycle G2/M phase arrest. Reconstitution of GADD45B can rescue the proliferation phenotype caused by EBV-miR-BART19-3p in EBVaGC cells, highlighting the role of GADD45B in EBV-miR-BART-driven Gastric cancer. Our study indicated Epstein-Barr Virus MicroRNA BART19-3p played an oncogenic role by a novel mechanism of inhibiting GADD45B in EBVaGC, which provides new insights and might be a potential therapeutic strategy for EBVaGC patients.

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Glis3 plays a crucial role in spermatogenesis

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