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Genome-wide mapping of SET-Nup214, mutant NPM1 (NPM1c), and CRM1-binding sites in human leukemia or mouse ES cell lines

ABSTRACT: Genome-wide mapping of SET-Nup214, mutant NPM1 (NPM1c), and CRM1-binding sites in human leukemia or mouse ES cell lines

PROVIDER: PRJNA525993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8695670.fastq.gz	Fastqsanger.gz
	SRR8695680.fastq.gz	Fastqsanger.gz
	SRR8695690.fastq.gz	Fastqsanger.gz
	SRR8695661.fastq.gz	Fastqsanger.gz
	SRR8695671.fastq.gz	Fastqsanger.gz

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Genome-wide mapping of SET-Nup214, mutant NPM1 (NPM1c), and CRM1-binding sites in human leukemia or mouse ES cell lines

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Project description:NPM1 is the most frequently mutated gene in cytogenetically normal acute myeloid leukemia (AML). In AML cells, NPM1 mutations result in abnormal cytoplasmic localization of the mutant protein (NPM1c). NPM1 mutations are founding genetic lesions, however it is unknown whether NPM1c is required to maintain the leukemic state. Here, we show that loss of NPM1c from the cytoplasm, either through nuclear relocalization or targeted degradation, results in downregulation of homeobox (HOX) genes, and differentiation and cell growth arrest of AML cells. Additionally, we show that HOX downregulation is the earliest transcriptional event following the loss of NPM1c from the cytoplasm, preceding and promoting differentiation. Finally, we show that XPO1 inhibition efficiently relocalizes NPM1c to the nucleus, enables differentiation and prolongs survival of Npm1c+ leukemic mice. We describe an exquisite dependency of NPM1-mutant AML cells on NPM1c, providing the rationale for the use of nuclear export inhibitors in AML with mutated NPM1.

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