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Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [ChIP-seq]

ABSTRACT: Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [ChIP-seq]

PROVIDER: PRJNA818625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18430238_1.fastq.gz	Fastqsanger.gz
	SRR18430238_2.fastq.gz	Fastqsanger.gz
	SRR18430239_1.fastq.gz	Fastqsanger.gz
	SRR18430239_2.fastq.gz	Fastqsanger.gz
	SRR18430240_1.fastq.gz	Fastqsanger.gz

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Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells

Project description:Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells

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Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [RNA-seq]

Project description:Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [RNA-seq]

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Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells.

Project description:Acute myeloid leukemia (AML) with mixed-lineage leukemia (MLL) gene rearrangement (MLLr) comprises a cellular hierarchy in which a subpopulation of cells serves as functional leukemia stem cells (LSCs). They are maintained by a unique gene expression program and chromatin states, which are thought to reflect the actions of enhancers. Here, we delineate the active enhancer landscape and observe pervasive enhancer malfunction in LSCs. Reconstruction of regulatory networks revealed a master set of hematopoietic transcription factors. We show that EP300 is an essential transcriptional coregulator for maintaining LSC oncogenic potential because it controls essential gene expression through modulation of H3K27 acetylation and assessments of transcription factor dependencies. Moreover, the EP300 inhibitor A-485 affects LSC growth by targeting enhancer activity via histone acetyltransferase domain inhibition. Together, these data implicate a perturbed MLLr-specific enhancer accessibility landscape, suggesting the possibility for disruption of the LSC enhancer regulatory axis as a promising therapeutic strategy in AML.

| S-EPMC10248086 | biostudies-literature

Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [RNA-seq]

Project description:Acute myeloid leukemia (AML) with MLL gene rearrangement (MLLr) comprises a cellular hierarchy in which subpopulations of cells with distinct immunophenotypes serve as functional leukemia stem cells (LSCs, c-Kit+) and mature AML cells (mAML, c-Kit-), respectively. They are maintained by a unique gene expression program and chromatin states, which are thought to reflect the actions of cis-regulatory elements with features of enhancers. Here, we delineate the active enhancer landscape and observe pervasive enhancer malfunction in MLLr LSCs. Reconstruction of regulatory networks revealed a master set of hematopoietic transcription factors (TFs). We show that EP300 is an essential transcriptional coregulator with these TFs for maintaining LSC oncogenic potential, as it controls essential gene expression through modulation of H3K27 acetylation and assessments of transcription factor dependencies. Moreover, the EP300 small molecule inhibitor A-485 affects LSC growth by targeting enhancer activity via histone acetyltransferase domain inhibition. Together, these data implicate a perturbed MLLr-specific enhancer accessibility landscape, suggesting the possibility for disruption of the LSC enhancer regulatory axis as a promising therapeutic strategy in AML.

2023-02-07 | GSE199786 | GEO

Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells [ChIP-seq]

2023-02-07 | GSE199129 | GEO

Expression data from conditionally immortalized MLL-AF9 and MLL-ENL hematopoietic progenitor cells following loss of MLL-fusion oncogene

Project description:Chromosomal translocations encoding the MLL-AF9 and MLL-ENL fusion transcription factors are prevalent in infant acute leukaemia and therapy-related leukaemia. In order to conditionally express the MLL-fusion oncogene in primary haematopoietic progenitor cells (HPC), retroviral delivery of the Tet-off expression system was used (Horton et al., Cancer Res, 2005). Treatment of the conditional cells with Doxycycline caused a decrease in MLL-AF9/ENL mRNA and protein expression, and resulted in terminal differentiation of the cells. By analysing global changes in gene expression after treatment of cells with Doxycycline we were able to identify a number of potential transcriptional target genes of the MLL-AF9 and MLL-ENL fusion oncogenes.

2014-12-01 | GSE59236 | GEO

Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-07 | GSE199788 | GEO

Controlled MLL-AF9 Expression in Human Induced Pluripotent Stem Cells Reveals MLL-AF9-specific Oncogene Program [hiMLLAF9_scRNAseq]

Project description:Controlled MLL-AF9 Expression in Human Induced Pluripotent Stem Cells Reveals MLL-AF9-specific Oncogene Program [hiMLLAF9_scRNAseq]

| PRJNA896573 | ENA

DNMT1 drives 4D genome rewiring during oncogene induced senescence

Project description:DNMT1 drives 4D genome rewiring during oncogene induced senescence

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Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

Project description:Fusion of the N-terminus of the mixed-lineage-leukemia (MLL) gene with various partner genes drives acute lymphoblastic leukemia (ALL). Despite the fusion proteins sharing some common attributes, transcriptome heterogeneity of MLL-fusion ALL is observed and the underlying mechanism and biological consequences are unknown. We compared the genome-wide occupancy of MLL-Af4 and MLL-AF9 in human ALL cells expressing FLAG-tagged fusion proteins. Although both oncoproteins retain the same MLL N-terminal domains that mediate chromatin binding, the two fusion proteins displayed largely non-overlapping binding profiles, with MLL-AF9 showing preferential binding at repetitive elements. The binding specificity of each fusion protein was associated with differential global gene activation distinguishing the two ALLs. A subset of prednisolone response genes were among the differentially regulated targets, and the resistance related genes were specifically upregulated in MLL-Af4/AF4 cells. These studies provide evidence that distinct chromatin occupancy of different MLL-fusion proteins is one driving force for transcriptome heterogeneity of MLL-fusion ALL, which could potentially result in the disparate therapeutic outcome of the disease.

2018-04-30 | GSE103947 | GEO

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