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RNA-seq analysis of transcriptomic changes in WT and MPHOSPH8 KO MOLM-13 leukemia cells

ABSTRACT: RNA-seq analysis of transcriptomic changes in WT and MPHOSPH8 KO MOLM-13 leukemia cells

PROVIDER: PRJNA634320 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13075709_1.fastq.gz	Fastqsanger.gz
	SRR13075709_2.fastq.gz	Fastqsanger.gz
	SRR13075710_1.fastq.gz	Fastqsanger.gz
	SRR13075710_2.fastq.gz	Fastqsanger.gz
	SRR13075711_1.fastq.gz	Fastqsanger.gz

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Analysis of MPHOSPH8 chromatin occupancy and MPHOSPH8-dependent gene expression in MOLM-13 leukemia cells

Project description:Analysis of MPHOSPH8 chromatin occupancy and MPHOSPH8-dependent gene expression in MOLM-13 leukemia cells

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RNA-seq analysis of transcriptomic changes in WT and MPHOSPH8 KO MOLM-13 leukemia cells

Project description:Human cancers including acute myeloid leukemia (AML) hijack epigenetic machinery to drive malignant self-renewal, whereas dysregulated epigenetic states also create selective and targetable liabilities. We performed domain-based CRISPR/Cas9 screens of human chromatin regulators and identified MPHOSPH8 (or MPP8), a component of the HUSH complex and repressor of LINE-1 retrotransposons, as a selective epigenetic dependency of AML cells. While dispensable for normal hematopoiesis, MPP8 loss inhibited AML initiation and maintenance by reactivating LINE-1 retrotransposons. Activation of endogenous or ectopic LINE-1 photocopied MPP8 loss, whereas blocking LINE-1 retrotransposition abrogated MPP8-deficiency-induced phenotypes. Reactivated LINE-1 retrotransposition increased DNA damage, activated cyclin-dependent kinase inhibitor p21 (or CDKN1A), and induced AML differentiation. Enhanced L1 suppression in AML stem cells is associated with therapy resistance and poor prognosis. Hence, while retrotransposons are historically recognized as sources of genetic instability and somatic mutations, we uncover an unexpected role for HUSH/MPP8 in promoting cancer by suppressing genomic transposable elements.

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Effect of FL-Fc-DM1 drug on gene expression of Molm-13 cells

Project description:To eliminate cell-cycle arrested AML cells, we developed a FL-Fc-DM1 drug by conjugating FLT3 liangd Fc fusion protein and mertansine. We used the Molm-13 cells as a AML model. The total mRNA of Molm-13 cells treated with different concentration of FL-Fc-DM1 were sequenced.

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ChIP-seq analysis of HA-KAT6A in MOLM-13 AML cells

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Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in leukemia cell line MOLM-13 cells and performed RNA-seq experiments to profile transcriptional changes upon FIS1 depletion.

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