Ontology highlight
ABSTRACT:
PROVIDER: PRJNA258409 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1553290_1.fastq.gz | Fastqsanger.gz | |||
| SRR1553290_2.fastq.gz | Fastqsanger.gz | |||
| SRR1553291_1.fastq.gz | Fastqsanger.gz | |||
| SRR1553291_2.fastq.gz | Fastqsanger.gz | |||
| SRR1553292_1.fastq.gz | Fastqsanger.gz |
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Project description:Recent sequencing-based experiments mapping ensemble interaction frequency among regulatory elements in cancer cells support the existence of complex topological assemblies of enhancers and promoters known as promoter-enhancer hubs or cliques. Yet, the prevalence of promoter-enhancer hubs in individual cells, factors regulating their dynamics and assembly, as well as their role in transcriptional dysregulation in cancer remain unclear. Here, we systematically integrated functional genomics, transcription factor screening, and optical mapping of promoter-enhancer interactions to identify key promoter-enhancer hubs, examine heterogeneity of their assembly, determine their regulators, and elucidate their role in gene expression control in individual triple negative breast cancer (TNBC) cells. Optical mapping of individual SOX9 and MYC alleles revealed the existence of frequent multiway interactions among gene promoters and enhancers within promoter-enhancer hubs. Our single-allele studies further demonstrated that lineage-determining SOX9 and signaling-dependent NOTCH1 transcription factors compact MYC and SOX9 promoter-enhancer hubs, respectively. Together, our findings suggest that promoter-enhancer hubs are dynamic and heterogeneous topological assemblies controlled by oncogenic transcription factors potentially in a cancer subtype-restricted manner to facilitate aberrant gene expression.
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Project description:High resolution mapping of enhancer-promoter interactions [ChIA-PET]
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Project description:Recent advances in high-resolution mapping of spatial interactions among regulatory elements support the existence of complex topological assemblies of enhancers and promoters known as enhancer-promoter hubs or cliques. Yet, organization principles of these multi-interacting enhancer-promoter hubs and their potential role in regulating gene expression in cancer remains unclear. Here, we systematically identified enhancer-promoter hubs in breast cancer, lymphoma, and leukemia. We found that highly interacting enhancer-promoter hubs form at key oncogenes and lineage-associated transcription factors potentially promoting oncogenesis of these diverse cancer types. Genomic and optical mapping of interactions among enhancer and promoter elements further showed that topological alterations in hubs coincide with transcriptional changes underlying acquired resistance to targeted therapy in T cell leukemia and B cell lymphoma. Together, our findings suggest that enhancer-promoter hubs are dynamic and heterogeneous topological assemblies with the potential to control gene expression circuits promoting oncogenesis and drug resistance.
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