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

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

PROVIDER: PRJNA532526 | 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
	SRR8887170.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]

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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.

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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.

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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.

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