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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

ABSTRACT: Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

PROVIDER: PRJNA686276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13271919_1.fastq.gz	Fastqsanger.gz
	SRR13271919_2.fastq.gz	Fastqsanger.gz
	SRR13271920_1.fastq.gz	Fastqsanger.gz
	SRR13271920_2.fastq.gz	Fastqsanger.gz
	SRR13271921_1.fastq.gz	Fastqsanger.gz

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

Project description:Dysregulated gene expression is one of the most prevalent features in human cancers. Here, we show that most subtypes of acute myeloid leukemia (AML) depend on the aberrant assembly of the MYB transcriptional co-activator complex. By rapid and selective peptidomimetic interference with the binding of CBP/P300 to MYB, but not CREB or MLL1, we find that the leukemic functions of MYB are mediated by CBP/P300-mediated co-activation of a distinct set of transcriptional factor complexes that are aberrantly assembled with MYB in AML cells. This therapeutic remodeling is accompanied by dynamic redistribution of CBP/P300 complexes to genes that control cellular differentiation and growth. Thus, aberrantly organized transcription factor complexes control convergent gene expression programs in AML cells. These findings establish a compelling strategy for pharmacologic reprogramming of oncogenic gene expression that supports its targeting for leukemias and other human cancers caused by dysregulated gene control.

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [ChIPseq]

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [ChIPseq]

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_MV411]

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_MV411]

| PRJNA686277 | ENA

Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

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Definition of aberrant MYB CBP/P300 complex in AML

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

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

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MYB-regulated pancreatic cancer secretome

Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.

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The AAA+ ATPAse RUVBL2 is essential for the oncogenic function of c-MYB in acute myeloid leukemia

Project description:Subtype-specific leukemia oncogenes drive aberrant gene expression profiles that converge on common essential mediators to ensure leukemia self-renewal and inhibition of differentiation. The transcription factor c-MYB functions as one such mediator in a diverse range of leukemias. Here we show that transcriptional repression of myeloid differentiation associated c-MYB target genes in AML is enforced by the AAA+ ATPAse RUVBL2. Silencing RUVBL2 expression resulted in increased binding of c-MYB to these loci and their transcriptional derepression. RUVBL2 inhibition induced AML cell apoptosis and severely impaired disease progression of established AML in engrafted mice. In contrast, such inhibition had little impact on normal hematopoietic progenitor differentiation. These data reveal a central mechanism governing inhibition of myeloid differentiation by c-MYB in AML. They also indicate that targeting the control of c-MYB function by RUVBL2 is likely to be a promising approach to developing future anti-AML therapies.

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