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Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [CUT&RUN]

ABSTRACT: Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [CUT&RUN]

PROVIDER: PRJNA1103835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28786368_1.fastq.gz	Fastqsanger.gz
	SRR28786368_2.fastq.gz	Fastqsanger.gz
	SRR28786369_1.fastq.gz	Fastqsanger.gz
	SRR28786369_2.fastq.gz	Fastqsanger.gz
	SRR28786370_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [CUT&RUN]

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.

2024-08-16 | GSE264706 | GEO

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [RNA-seq]

2024-08-16 | GSE264707 | GEO

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [ChIP-seq]

2024-08-16 | GSE264705 | GEO

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells

Project description:Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells

| PRJNA1103827 | ENA

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [RNA-seq]

Project description:Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [RNA-seq]

| PRJNA1103834 | ENA

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [ChIP-seq]

Project description:Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells [ChIP-seq]

| PRJNA1103829 | ENA

Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells

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

2024-08-16 | GSE264708 | GEO

A fine kinetic balance of interactions directs transcription factor hubs to genes [Cut and Run]

Project description:A fine kinetic balance of interactions directs transcription factor hubs to genes [Cut and Run]

| PRJNA1100527 | ENA

A fine kinetic balance of interactions directs transcription factor hubs to genes [Cut and Run]

Project description:Eukaryotic gene regulation relies on the binding of sequence-specific transcription factors (TFs). TFs bind chromatin transiently yet occupy their target sites by forming high-local concentration microenvironments (hubs and condensates) that increase the frequency of binding events. Despite their ubiquity, such microenvironments have been difficult to study in endogenous contexts due to technical limitations. Here, we overcome these limitations and investigate how hubs drive TF occupancy at their targets. Using a DNA binding perturbation to a hub-forming TF, Zelda, in Drosophila embryos, we find that hub properties, including the stability and frequencies of associations to targets, are key determinants of TF occupancy. Our data suggest that hub targeting is driven not just by specific DNA motif recognition, but also by a fine-tuned kinetic balance of interactions between TFs and their co-binding partners.

2024-04-15 | GSE263999 | GEO

ecDNA hubs drive cooperative intermolecular oncogene expression [ChIP]

Project description:Extrachromosomal DNA (ecDNA) is prevalent in human cancers and mediates high oncogene expression through gene amplification and altered gene regulation. Gene induction typically involves cis regulatory elements that contact and activate genes on the same chromosome. Here we show that ecDNA hubs, clusters of ~10-100 ecDNAs within the nucleus, enable intermolecular enhancer-gene interactions to promote oncogene overexpression in trans. ecDNAs encoding multiple distinct oncogenes form hubs in diverse cancer cell types and primary tumors. Each ecDNA is more likely to transcribe the oncogene when spatially clustered with additional ecDNAs. ecDNA hubs are tethered by the BET protein BRD4 in a MYC-amplified colorectal cancer cell line. BET inhibitor JQ1 disperses ecDNA hubs and preferentially inhibits ecDNA-based oncogene transcription. A BRD4-bound promoter in PVT1 is ectopically fused to MYC and duplicated in ecDNA, receiving promiscuous enhancer input to drive potent MYC expression. PVT1 promoter on a heterologous episome suffices to mediate gene activation in trans by ecDNA hubs in a JQ1-sensitive manner. Systematic CRISPRi silencing of ecDNA enhancers reveal intermolecular enhancer-gene activation among multiple oncogene loci amplified on distinct ecDNAs. Together, these results demonstrate that ecDNA hubs are protein-tethered clusters of ecDNAs which enable intermolecular transcriptional regulation. ecDNA hubs may act as units of oncogene function, cooperative evolution, and potential targets for cancer therapy.

2020-11-25 | GSE159972 | GEO

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