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Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

ABSTRACT: Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

PROVIDER: PRJNA601312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10897088.fastq.gz	Fastqsanger.gz
	SRR10897089.fastq.gz	Fastqsanger.gz
	SRR10897090.fastq.gz	Fastqsanger.gz
	SRR10897091.fastq.gz	Fastqsanger.gz

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Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

| PRJNA532532 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

| PRJNA532531 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

| PRJNA532526 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE129701 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE143691 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE129700 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

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

2020-04-01 | GSE129702 | GEO

MLL4 establishes super-enhancers and broad H3K4me3 for tumor-suppressive function

Project description:Clusters of enhancers called super-enhancers are associated with gene activation. Broad trimethyl histone H3 lysine 4 (H3K4me3) often defines actively transcribed tumor suppressor genes. However, how these epigenetic signatures are regulated for tumor suppression is poorly understood. Here, we show that brain-specific knockout of the H3K4 methyltransferase MLL4 (aka KMT2D) in mice spontaneously induces cerebellar tumors in brain while indirectly increasing expression of oncogenic programs, such as Ras activators and Notch pathway components. Mll4 loss caused widespread impairment of super-enhancers and broad H3K4me3. Notably, Mll4 loss reduced super-enhancer and broad H3K4me3 signals in tumor suppressor genes co-marked by both signatures, including Dnmt3a and Bcl6. MLL4 upregulates DNMT3A-mediated DNA methylation to downregulate expression of Ras activators and increases Bcl6 expression to suppress the Notch pathway. These findings suggest an unanticipated epigenetic tumor-suppressive mechanism in which MLL4 is required for establishing super-enhancers and broad H3K4me3 for anti-tumor programs in normal cells.

2018-11-13 | GSE95626 | GEO

Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

Project description:Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

| PRJNA636364 | ENA

Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

Project description:Chromosomal translocations are important drivers of haematological malignancies whereby proto-oncogenes are activated by juxtaposition with super-enhancers, often called super-enhancer hijacking. We analysed the epigenomic consequences of rearrangements between the enhancers of the immunoglobulin heavy chain locus (IGH) and proto-oncogene CCND1 that are common in B-cell malignancies. By integrating BLUEPRINT epigenomic data with DNA breakpoint detection, we characterised the normal chromatin landscape of the human IGH locus and its dynamics after pathological genomic rearrangement. We detected an H3K4me3 broad domain (BD) within the IGH locus of healthy B-cells that was absent in samples with IGH-CCND1 translocations. The appearance of H3K4me3-BD over CCND1 in the latter was associated with overexpression and extensive chromatin accessibility of this locus. We observed similar cancer-specific H3K4me3-BDs associated with super-enhancer hijacking of other common oncogenes in B-cell (MAF, MYC and FGFR3) and in T-cell malignancies (LMO2, TLX3 and TAL1). Our analysis suggests that H3K4me3-BDs are created by super-enhancers and supports the new concept of epigenomic translocation, where the relocation of H3K4me3-BDs accompanies the translocation of super-enhancers.

2020-08-12 | GSE151556 | GEO

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