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Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

ABSTRACT: Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

PROVIDER: PRJNA521224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8539820_1.fastq.gz	Fastqsanger.gz
	SRR8539820_2.fastq.gz	Fastqsanger.gz
	SRR8539830_1.fastq.gz	Fastqsanger.gz
	SRR8539830_2.fastq.gz	Fastqsanger.gz
	SRR8539840_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.

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Project description:The histone-3 lysine-4 methyltransferase KMT2D is frequently mutated in human cancers. However, knowledge of its role in the initiation and maintenance of acute myeloid leukemia (AML) is incomplete. Here, we show that KMT2D is generally downregulated in human AML. Using shRNA and CRISPR/Cas9 technologies, we show that Kmt2d loss, by cooperating with Trp53 and Nf1 loss, promoted mouse acute myeloid leukemogenesis through a differentiation block of hematopoietic stem and progenitor cells. Furthermore, using a doxycycline-induced shRNA system, we show that restoring Kmt2d impairs AML maintenance. Multi-omics analyses of Kmt2d-deficient and -restored AML cells showed that Kmt2d, via histone methyltransferase activity and chromatin remodeling, epigenetically regulates the expression of genes controlling hematopoietic stem cell differentiation. Lastly, we showed that 3-Deazaneplanocin A, a histone methyltransferase EZH2 inhibitor, could specifically repress Kmt2d-deficient AML cell growth and reverse pro-leukemia programs. Thus, our study indicate Kmt2d is a tumor suppressor, whose downregulation promotes AML development through differentiation blockage.

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