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Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network [ChIP-seq]

ABSTRACT: Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network [ChIP-seq]

PROVIDER: PRJNA951706 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24049112_1.fastq.gz	Fastqsanger.gz
	SRR24049112_2.fastq.gz	Fastqsanger.gz
	SRR24049113_1.fastq.gz	Fastqsanger.gz
	SRR24049113_2.fastq.gz	Fastqsanger.gz
	SRR24049114_1.fastq.gz	Fastqsanger.gz

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Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network

Project description:Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network

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Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network [ChIP-seq]

Project description:Enhancers are non-coding genomic features that regulate the transcriptional output of their target genes. Their dysregulation has been associated with various diseases including cancer. However, identification and characterisation of non-coding mutations that are relevant for tumorigenesis and prognosis remain a major challenge. Here we present the detection and characterisation of enhancer mutations in a genome-wide analysis of three lung cancer subtypes. We carefully define lung tissue-specific enhancers across the genome by integrating novel experimental data and reference public datasets of epigenomic signatures from eight lung cell lines and primary tissue. We observe that in lung cancer, the mutation burden at enhancers and exons is similar, whereas their corresponding mutation signatures show stark differences. Our results indicate that recurrent mutations in individual enhancers significantly impact the expression of target genes with potential relevance for prognosis. We also demonstrate that the genes enriched for mutated enhancers recurrently converge on the regulation of key biological process and pathways.

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Project description:In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cellM-bM-^@M-^Ys transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. Further analysis of genome-wide binding identified MYB and its histone acetylase binding partner CBP as core components of the TAL1 complex and of the TAL1-mediated feed-forward auto-regulatory loop that drives T-ALL. Furthermore, MYB and CBP occupy endogenous MYB binding sites in the majority of super-enhancer sites found in T-ALL cells. Thus, our study reveals a new mechanism for the generation of super-enhancers in malignant cells involving the introduction of somatic indel mutations within non-coding sequences, which introduce aberrant binding sites for the MYB master transcription factor. ChIP-Seq for transcription factors and co-factors in T cell acute lymphoblastic leukemia cell lines

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Enhancer somatic mutations with functional impact in lung cancers identified by leveraging the tissue-specific enhancer-target genes regulatory network

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An Oncogenic Super-Enhancer Formed through Somatic Mutation of a Noncoding Intergenic Element

Project description:In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cell’s transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. Further analysis of genome-wide binding identified MYB and its histone acetylase binding partner CBP as core components of the TAL1 complex and of the TAL1-mediated feed-forward auto-regulatory loop that drives T-ALL. Furthermore, MYB and CBP occupy endogenous MYB binding sites in the majority of super-enhancer sites found in T-ALL cells. Thus, our study reveals a new mechanism for the generation of super-enhancers in malignant cells involving the introduction of somatic indel mutations within non-coding sequences, which introduce aberrant binding sites for the MYB master transcription factor.

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Project description:Genomic material within the nucleus is folded into successive layers in order to package and organize the long string of linear DNA. This hierarchical level of folding is closely associated with transcriptional regulation and DNA replication. Genes within the same folding domain demonstrate similar expression and histone-modification profiles1. Therefore, boundaries separating different domains have important roles in reinforcing the stability of these domain-wide features. Indeed, domain boundary disruptions in human genetic disorders2,3 or human cancers lead to misregulation of certain genes4,5, due to de novo enhancer exposure to promoters. However, the frequency of boundary disruptions in human cancers, and whether there are recurrently affected boundaries in specific cancer types, remains unclear. Here, to understand effects and distributions of somatic structural variations (SVs) across TADs, we utilized 288,457 high-confidence somatic structural variations from 2658 high-coverage whole genome sequencing datasets across various cancer types. We comprehensively profiled structural variations effects on the domain boundaries and the regulation of genes in human cancers. Notably, most of the TAD disruptions do not result in appreciable changes in nearby gene expression where more than 2-fold expression change was observed in only 14% of regions with the boundary deletions. In addition, we demonstrated that SV types affect TADs differently, specifically, complex rearrangements drastically change chromatin folding maps in the cancer genomes.

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