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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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ChIP-seq analysis of H3K4me3, H3K9me3 and MPHOSPH8 in MOLM-13 cells

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RNA-seq of MOLM-13 acute myeloid leukemia cell line treated with FIDAS-5

Project description:MOLM-13 acute myeloid leukemia cells were treated with 3 µM FIDAS-5 methionine S-adenosyltransferase 2A (MAT2A) inhibitor or 0.1% DMSO as control for 48 hours

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

Project description:ChIP-seq analysis of MOLM-13 human leukemia cells with overexpression of WT KAT6A with HA tag.

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RNA-seq analysis of Molm-13 cell with GADD45g overexpressed

Project description:The growth arrest and DNA-damage induced 45 gamma (GADD45g) is rapidly induced by various physiological and environmental stresses associated with growth arrest. GADD45g has been observed implicated in cell survival, apoptosis, senescence, cell cycle regulation and DNA repair in a variety of human solid tumor types, acting as either tumor promoter or tumor suppressor. To date, the role of GADD45g in hematopoietic malignancies remains completely unknown. Here, we transduced Molm-13 cells with lentiviral vectors expressing doxycycline-inducible GADD45g. Molm-13 cells with dox administration or not were collected for RNA-seq.

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Transcriptional profiling of MOLM-13 AML cells following KAT6A CRISPR targeting

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ChIP-seq analysis of H3K4me3, H3K9me3 and MPHOSPH8 in MOLM-13 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.

2018-06-01 | GSE114111 | GEO

Mitochondrial Fission 1 (FIS1) knockdown effect on the H3K27Ac status of leukemia cell line MOLM-13 cells

Project description:To examine if loss of FIS1 would alter the H3K27Ac status of leukemic cells, we used shRNA to knock down the expression of FIS1 in leukemic cell line MOLM-13 cells and performed H3K27Ac CHIP-seq to characterize any changes in the H3K27Ac marks upon loss of FIS1.

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