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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [ChIP-Seq]

ABSTRACT: A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [ChIP-Seq]

PROVIDER: PRJNA745187 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15089639.fastq.gz	Fastqsanger.gz
	SRR15089640.fastq.gz	Fastqsanger.gz
	SRR15089641.fastq.gz	Fastqsanger.gz
	SRR15089642.fastq.gz	Fastqsanger.gz

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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [RNA-Seq]

Project description:Acute myeloid leukemias (AMLs) with the NUP98-NSD1 or MLL gene rearrangement (MLL-r) share transcriptomic profiles featured with stemness-related gene signatures and display poor prognosis in the clinic. However, the molecular underpinnings of AML aggressiveness and stemness remain far from clear. Here, we report that the enzymatic activity of Polycomb Repressive Complex 2 (PRC2) is crucial for maintenance of tumorigenicity in NUP98-NSD1+ AML, consistent to its role in MLL-r AML. Transcriptomic analysis revealed Kdm5b, a lysine demethylase gene carrying the “bivalent domain” chromatin feature in AML, to be directly repressed by PRC2. While ectopic expression of Kdm5b suppressed AML growth, its depletion in AML not only promoted tumorigenicity but also significantly attenuated anti-AML effects by PRC2 inhibitors, thus demonstrating an involvement of the PRC2-|Kdm5b axis for AML oncogenesis. Lower KDM5B expression is positively correlated with poorer prognosis of human AML patients. RNA-seq, ChIP-seq and CUT&RUN based genomic profilings also showed that Kdm5b directly binds to and represses AML stemness genes. In contrast to an essential involvement for its various chromatin-associating domains, Kdm5b’s demethylase function was found to be dispensable for AML suppression, indicating a scaffold role in assembling gene-repressive complexes. Collectively, this study describes a molecular axis involving histone modifiers (PRC2 and Kdm5b) for sustaining the malignant features of AML, implicative of potential therapeutics.

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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [ChIP-Seq]

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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [CUT&RUN]

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Project description:A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia

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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [CUT&RUN]

Project description:A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [CUT&RUN]

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Project description:A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [RNA-Seq]

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A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia

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