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Engineered extrachromosomal oncogene amplifications promote tumorigenesis (RNA-Seq)

ABSTRACT: Engineered extrachromosomal oncogene amplifications promote tumorigenesis (RNA-Seq)

PROVIDER: PRJNA1100544 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28701947_1.fastq.gz	Fastqsanger.gz
	SRR28701947_2.fastq.gz	Fastqsanger.gz
	SRR28701948_1.fastq.gz	Fastqsanger.gz
	SRR28701948_2.fastq.gz	Fastqsanger.gz
	SRR28701949_1.fastq.gz	Fastqsanger.gz

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Project description:Focal gene amplifications are among the most common cancer-associated mutations, but their evolution and contribution to tumorigenesis have proven challenging to recapitulate in primary cells and model organisms. Here we describe a general strategy to engineer large (>1 Mbp) focal amplifications mediated by extrachromosomal circular DNAs (ecDNAs) in a spatiotemporally controlled manner in cells and in genetically engineered mice. By coupling ecDNA formation with expression of selectable markers, we track the dynamics of ecDNA-containing cells under physiological conditions and in the presence of specific selective pressures. We also apply this approach to generate mice harboring Cre-inducible Myc- and Mdm2-containing ecDNAs analogous to those occurring in human cancers. We show that the engineered ecDNAs spontaneously accumulate in primary cells derived from these animals, promoting their proliferation, immortalization, and transformation. Finally, we demonstrate the ability of Mdm2-containing ecDNAs to promote tumor formation in an autochthonous mouse model of hepatocellular carcinoma.

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Functional enhancers shape extrachromosomal oncogene amplifications

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Engineered extrachromosomal oncogene amplifications promote tumorigenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Modeling cellular pliancy-dependent oncogene-induced signaling and chemotherapeutic response during breast tumorigenesis

Project description:Modeling cellular pliancy-dependent oncogene-induced signaling and chemotherapeutic response during breast tumorigenesis

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Circular extrachromosomal DNA drives massive oncogene expression and chromatin accessibility

Project description:Oncogenes are commonly amplified on extrachromosomal DNA particles (ecDNA) in cancer, but our understanding of the structure of ecDNA and its impact on gene regulation is limited. We integrated ultrastructural imaging, long range-optical mapping, and computational analysis of whole genome sequencing to demonstrate unequivocally that ecDNA is circular. Pan-cancer analyses reveal that the oncogenes encoded on ecDNA are among the most highly expressed genes in the transcriptome of tumours, linking elevated copy with very high levels of transcription. Quantitative assessment of the chromatin state, including ATAC-seq to map the accessible genome and ATAC-see to examine spatial distribution of open chromatin, reveal that while ecDNA is chromatinized, it lacks higher order compaction typical of chromosomes. In fact, ecDNA contains the most accessible DNA in the tumour genome. Using chromosome conformation capture technologies and CRISPR interference, we reveal the differential organization of active chromatin in cancer that is dictated by the circular shape of ecDNA. Lastly, we develop comprehensive maps that provide new insight into how circular ecDNA structure determines oncogene function, bridging ecDNA biology with modern cancer genomics and epigenetics.

2019-12-31 | GSE131956 | GEO

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