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Widespread perturbation of ETS factor binding sites in cancer

ABSTRACT: Widespread perturbation of ETS factor binding sites in cancer

PROVIDER: PRJNA903909 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22361262.fastq.gz	Fastqsanger.gz
	SRR22361263.fastq.gz	Fastqsanger.gz
	SRR22361264.fastq.gz	Fastqsanger.gz
	SRR22361265.fastq.gz	Fastqsanger.gz
	SRR22361266.fastq.gz	Fastqsanger.gz

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Widespread perturbation of ETS factor binding sites in cancer

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Project description:Although >90% of somatic mutations reside in non-coding regions, few have been reported as cancer drivers. To predict driver non-coding variants (NCVs), we present a novel transcription factor (TF)-aware burden test (TFA-BT) based on a model of coherent TF function in promoters. We applied our TFA-BT to NCVs from the Pan-Cancer Analysis of Whole Genomes cohort and predicted 2,555 driver NCVs in the promoters of 813 genes across 20 cancer-types. These genes are enriched in cancer-related gene ontologies, essential genes, and genes associated with cancer prognosis. We found that 765 candidate driver NCVs alter transcriptional activity, 510 lead to differential binding of TF-cofactor regulatory complexes, and that they primarily impact the binding of ETS factors. Finally, we show that different NCVs within a promoter often affect transcriptional activity through shared mechanisms. Our integrated computational and experimental approach shows that cancer NCVs are widespread and that ETS factors are commonly disrupted.

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Widespread perturbation of ETS factor binding sites in cancer.

Project description:Although >90% of somatic mutations reside in non-coding regions, few have been reported as cancer drivers. To predict driver non-coding variants (NCVs), we present a transcription factor (TF)-aware burden test based on a model of coherent TF function in promoters. We apply this test to NCVs from the Pan-Cancer Analysis of Whole Genomes cohort and predict 2555 driver NCVs in the promoters of 813 genes across 20 cancer types. These genes are enriched in cancer-related gene ontologies, essential genes, and genes associated with cancer prognosis. We find that 765 candidate driver NCVs alter transcriptional activity, 510 lead to differential binding of TF-cofactor regulatory complexes, and that they primarily impact the binding of ETS factors. Finally, we show that different NCVs within a promoter often affect transcriptional activity through shared mechanisms. Our integrated computational and experimental approach shows that cancer NCVs are widespread and that ETS factors are commonly disrupted.

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Widespread perturbation of ETS factor binding sites in cancer

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

2023-01-09 | GSE222436 | GEO

Shear stress switches the association of endothelial enhancers from ETV/ETS to KLF transcription factor binding sites

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2015-03-30 | GSE59402 | GEO

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