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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [RNA-seq]

ABSTRACT: Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [RNA-seq]

PROVIDER: PRJNA999347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25442616.fastq.gz	Fastqsanger.gz
	SRR25442617.fastq.gz	Fastqsanger.gz
	SRR25442618.fastq.gz	Fastqsanger.gz
	SRR25442619.fastq.gz	Fastqsanger.gz
	SRR25442620.fastq.gz	Fastqsanger.gz

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

Project description:Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

| PRJNA999344 | ENA

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [RNA-seq]

Project description:Gain-of-function mutations in the chromatin ‘reader’ ENL, identified in AML and Wilms tumor, have been shown to induce aberrant formation of transcriptional condensates in cellular systems. However, the precise role of these mutations and their condensate forming property in tumorigenesis remains unclear. By creating a conditional knock-in mouse model for the most prevalent ENL mutation, we establish ENL mutant as a bona fide oncogenic driver of acute myeloid leukemia in vivo. Heterozygous expression of ENL mutant perturbs the normal hematopoietic hierarchy and results in the aberrant expansion of myeloid progenitors with increased self-renewal property. Furthermore, the ENL mutant remodels histone modifications to alter differentiation processes and drive oncogenic gene expression during hematopoietic development. Importantly, targeted point mutagenesis to disrupt the condensate formation property completely abolishes ENL mutant’s oncogenic function in hematopoietic stem and progenitor cells (HSPCs). Lastly, short-term treatment with a small molecule inhibitor that blocks the acetyl-binding activity of ENL mutant reverts its impact on chromatin and significantly delays leukemia development in mice. Our studies reveal the crucial biological function of mutation-induced transcriptional condensates in chromatin regulation and cancer in vivo and provide proof-of-concept for targeting of pathogenic condensates as a promising therapy for certain cancers.

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

Project description:Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

| PRJNA999348 | ENA

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

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

2024-04-14 | GSE239470 | GEO

Targeting redox-sensitive MBD2-NuRD condensate for tumor therapy [ATAC-seq]

Project description:Transcriptional silencing of hypermethylated tumor suppressor genes is a hallmark of tumorigenesis, though the underlying mechanism remains enigmatic. In this study, we find Methyl-CpG-binding domain protein 2 (MBD2) forms nuclear condensate in diverse cancer cells, where it assembles and navigates the chromatin remodeler NuRD complex to these gene loci for transcriptional suppression, thus fueling tumor growth. Disturbance of MBD2 condensate reduces the level of NuRD complex-specific proteins, destabilizes heterochromatin foci, facilitates chromatin relaxation, and consequently impedes tumor progression. We demonstrate that MBD2 condensate is redox sensitive mediated by Cys359. Prooxidative interventions disperse MBD2-NuRD condensate, thereby alleviating the transcriptional repression of tumor suppressor genes. Our findings illuminate a hitherto unappreciated function of MBD2 condensate in sustaining a repressive chromatin state essential for cancer cell proliferation and suggest an oxidative stress targeting approach for malignancies with excessive MBD2 condensate.

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Targeting redox-sensitive MBD2-NuRD condensate for tumo therapy [RNA-Seq]

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Targeting redox-sensitive MBD2-NuRD condensate for tumor therapy [ChIP-Seq]

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2024-05-27 | GSE243867 | GEO

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