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CD37 Regulates the Self-Renewal of Leukemic Stem Cells via Integrin Mediated Signaling in Acute Myeloid Leukemia

ABSTRACT: CD37 Regulates the Self-Renewal of Leukemic Stem Cells via Integrin Mediated Signaling in Acute Myeloid Leukemia

PROVIDER: PRJNA1237354 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32744235_1.fastq.gz	Fastqsanger.gz
	SRR32744235_2.fastq.gz	Fastqsanger.gz
	SRR32744236_1.fastq.gz	Fastqsanger.gz
	SRR32744236_2.fastq.gz	Fastqsanger.gz
	SRR32744237_1.fastq.gz	Fastqsanger.gz

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CD37 Regulates the Self-Renewal of Leukemic Stem Cells via Integrin Mediated Signaling in Acute Myeloid Leukemia

Project description:Leukemic stem cells (LSCs) are a small subset of leukemia cells which drive leukemia initiation and maintenance. Herein, we report that CD37, a member of transmembrane 4 superfamily (TM4SF), regulates the survival of acute myeloid leukemia (AML) cells as well as the self-renewal of AML LSCs. The downregulation of CD37 retarded proliferation and increased apoptosis in human AML cell lines THP-1 and OCI-AML2. Deficiency of CD37 in vivo had a minimal effect on normal hematopoiesis, but significantly impeded leukemia maintenance and propagation, which led to increased apoptosis and decreased cell cycle entry in AML blasts as well as impaired colony formation and declined frequency of AML LSCs in the serial transplantation. Furthermore, CD37 interacted with integrin α4β7 and activated PI3K-AKT pathway mediated by integrin signaling. Our study provides novel insights for targeted therapy of AML, indicating CD37 as a safe and effective target for immunotherapy.

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Project description:Recent studies have indicated that the histone 3 lysine 27 (H3K27me2/3) demethylase KDM6B (JMJD3) is frequently upregulated in a myriad of blood disorders including myelodysplastic syndrome (MDS), T-cell acute lymphoblastic leukemia (T-ALL), and multiple myeloma (MM) suggesting it may have important functions in the pathogenesis of hematopoietic cancers. Here, we sought to determine the role of Kdm6b in hematopoietic stem cell (HSC) fate decisions under normal and malignant conditions to evaluate its potential as a therapeutic target. We show that loss of Kdm6b leads to a significant reduction in phenotypic and functional HSCs in adult mice, and that Kdm6b is necessary for HSC self-renewal in response to inflammatory, genotoxic and oncogenic stress. Additionally, we show that loss of Kdm6b in HSCs leads to a stress-response gene expression signature in native HSCs that is independent of its demethylase activity. Loss of Kdm6b lead to increased expression of a subset of genes implicated in HSC quiescence (e.g. Fos, Jun, Ier2, Dusp1, Zfp36). Upon inflammatory or replicative stress, HSCs deficient for Kdm6b are not able to efficiently resolve this gene expression program, leading to increased quiescence and a self-renewal block, forcing them to differentiate. These findings show that Kdm6b is necessary for self-renewal of normal and leukemic stem cells, and suggest inhibiting Kdm6b in blood cancers in the presence of proliferative agents may force differentiation and eventual depletion of leukemic stem cells.

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