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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

ABSTRACT: Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

PROVIDER: PRJNA999344 | 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 [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 [RNA-seq]

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling

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

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Project description:ENL is an epigenetic acetylation reader and represents the most frequently mutated epigenetic regulator in Wilms tumor. In this study, we established an in vivo mouse model with the ENL hotspot mutation Enl-T1. Here we performed RNA sequencing (RNA-seq) analysis for human embryonuc kidney cell line HEK293 with ENL-WT, T1 or T2 to study the transcriptional changes induced by ENL mutations and whether those alterations can be rescued by treating the cells with the specific ENL inhibitor TDI-11055.

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