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Landscape of enhancer disruption and functional screen in melanoma [CRISPRi]

ABSTRACT: Landscape of enhancer disruption and functional screen in melanoma [CRISPRi]

PROVIDER: PRJNA865708 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20789793.fastq.gz	Fastqsanger.gz
	SRR20789794.fastq.gz	Fastqsanger.gz
	SRR20789795.fastq.gz	Fastqsanger.gz
	SRR20789796.fastq.gz	Fastqsanger.gz
	SRR25756508.fastq.gz	Fastqsanger.gz

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Landscape of enhancer disruption and functional screen in melanoma [CRISPRi]

Project description:The high mutation rate across the whole melanoma genome provides a major challenge in stratifying true driver events from the background mutations. Many non-coding recurrent events, such as those occurred in enhancer, can shape tumor evolution, emphasizing the importance in systematically deciphering enhancer disruptions in melanoma. Here, we leveraged 297 melanoma whole-genome sequencing (WGS) samples to prioritize highly recurrent regions (HRRs). By performing a genome-scale CRISPR interference (CRISPRi) screen on HRR-associated enhancers in melanoma cells, we identified 66 significant hits which could have tumor-suppressive roles. These functional enhancers show unique mutational patterns independent of classical significantly mutated genes in melanoma. Target gene analysis for the essential enhancers revealed many known and hidden mechanisms underlying melanoma development. We demonstrated that a super enhancer element could modulate melanoma cell proliferation by targeting MEF2A and another distal enhancer was able to sustain PTEN tumor-suppressive potential via long-range interaction. Our study established a catalogue of crucial enhancers and their target genes in melanoma development and progression, which illuminates the identification of novel mechanism of dysregulation for melanoma driver genes and new therapeutic targeting strategy.

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Project description:Here, we leveraged 297 melanoma whole-genome sequencing (WGS) samples to prioritize highly recurrent regions (HRRs). By performing a genome-scale CRISPR interference (CRISPRi) screen on HRR-associated enhancers in melanoma cells, we identified 66 significant hits which could have tumor-suppressive roles. These functional enhancers show unique mutational patterns independent of classical significantly mutated genes in melanoma. Target gene analysis for the essential enhancers revealed many known and hidden mechanisms underlying melanoma growth. Utilizing extensive functional validation experiments, we demonstrated that a super enhancer element could modulate melanoma cell proliferation by targeting MEF2A and another distal enhancer was able to sustain PTEN tumor-suppressive potential via long-range interaction.

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