Landscape of enhancer disruption and functional screen in melanoma [4C-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA865706 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20791497_1.fastq.gz | Fastqsanger.gz | |||
| SRR20791497_2.fastq.gz | Fastqsanger.gz | |||
| SRR20791498_1.fastq.gz | Fastqsanger.gz | |||
| SRR20791498_2.fastq.gz | Fastqsanger.gz |
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Project description:Landscape of enhancer disruption and functional screen in melanoma
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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:Landscape of enhancer disruption and functional screen in melanoma [HiChIP]
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Project description:Landscape of enhancer disruption and functional screen in melanoma [CRISPRi]
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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.
2023-10-10 | GSE210424 | GEO
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.
2023-10-11 | GSE210423 | GEO
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.
2023-10-11 | GSE210422 | GEO
Project description:Enhancer looping governs gene regulatory circuitry but is challenging to detect. Here we present Tri-4C, an ultrafine mapping method for distal chromatin contacts using triple restriction enzyme (RE) digestion. Tri-4C identifies enhancer loops that are undetectable by current single RE- based methods and reveals quantitative loop strengths in enhancer interaction networks underlying dynamic gene control. This multi-RE approach may be applied to general 3C-derived methods for accurate detection of enhancer loops.
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Project description:BackgroundThe high mutation rate throughout the entire melanoma genome presents a major challenge in stratifying true driver events from the background mutations. Numerous recurrent non-coding alterations, such as those in enhancers, can shape tumor evolution, thereby emphasizing the importance in systematically deciphering enhancer disruptions in melanoma.ResultsHere, we leveraged 297 melanoma whole-genome sequencing samples to prioritize highly recurrent regions. By performing a genome-scale CRISPR interference (CRISPRi) screen on highly recurrent region-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 reveal many known and hidden mechanisms underlying melanoma growth. Utilizing extensive functional validation experiments, we demonstrate that a super enhancer element could modulate melanoma cell proliferation by targeting MEF2A, and another distal enhancer is able to sustain PTEN tumor-suppressive potential via long-range interactions.ConclusionsOur study establishes a catalogue of crucial enhancers and their target genes in melanoma growth and progression, and illuminates the identification of novel mechanisms of dysregulation for melanoma driver genes and new therapeutic targeting strategies.
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Project description:Defining Essential Enhancer for Pluripotent stem cells using Features Oriented CRISPR-Cas9 Screen (4C-Seq)
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