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3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [ChIP-Seq]

ABSTRACT: 3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [ChIP-Seq]

PROVIDER: PRJNA948422 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23957804.fastq.gz	Fastqsanger.gz
	SRR23957805.fastq.gz	Fastqsanger.gz
	SRR23957806.fastq.gz	Fastqsanger.gz
	SRR23957807.fastq.gz	Fastqsanger.gz
	SRR23957808.fastq.gz	Fastqsanger.gz

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3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [HiChIP]

Project description:Enhancer hijacking, caused by structural alterations, is a common cancer driver event that causes aberrant expression of oncogenes. Unfortunately, enhancer hijacking is difficult to detect due to the complexity of the cancer genome. Here we propose a simple yet robust strategy HAPI (Highly Active Promoter Interactions) to identify and characterize such events by following two rules: 1) oncogenes subject to enhancer hijacking should be potentially highly regulated by enhancers, 2) the hijacked enhancers should contribute an appreciable proportion of an oncogene’s overall enhancer activity. Applying this strategy to HiChIP data we and others generated in 34 cancer cell lines, we identified known enhancer hijacking events and uncovered novel enhancers hijacked by known or potentially novel oncogenes such as CCND1, ETV1, ID4, and NKX2-5, which we validated using CRISPRi assays and RNA-seq analysis. Furthermore, we found that complex enhancer hijacking events connecting genes and enhancers from multiple chromosomal segments are often caused by the formation of extrachromosomal circular DNA (ecDNA). Focusing on ecDNAs harboring the MYC oncogene, one of the most common gene targets of ecDNA, we found that these ecDNAs often stitch additional genes such as CDX2, ERBB2, and NFIB from other chromosomes to the MYC locus. These genes heavily hijack MYC enhancers for their activation, a novel insight into ecDNA biology, suggesting alternative therapeutic targets for MYC ecDNAs. Our study provides an efficient strategy to detect enhancer hijacking events, and more importantly reveals novel mechanisms underlying oncogene activation caused by simple or complex structural alterations.

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3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [RNA-Seq]

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3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [HiChIP]

Project description:3D genomics analysis identifies enhancer hijacking caused by structural alterations and extrachromosomal circular DNA formation [HiChIP]

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Project description:Extrachromosomal circular DNA (eccDNA) is double-stranded circular DNA that is derived from but independent of chromosomal DNA. Owing to its nonchromosomal inheritance, eccDNA facilitates the amplification of oncogenes and expedites the process of genome evolution in tumor. However, the role of eccDNA in RB remains enigmatic. We combined Circle-Seq and RNA-Seq to identified crucial extrachromosomal circular oncogene amplicons. Herein, we revealed that extrachromosomal circular SUZ12 amplicon regulates H3K27me3 modification during the oncogenic progression of retinoblastoma. Conclusively, our study initially delineated an integrated picture of the eccDNA landscape in retinoblastoma and unveiled a novel SUZ12-containing eccDNA/H3K27me3 oncogenic mechanism where eccDNA dictates retinoblastoma progression through regulating transcription levels of linear DNA.

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