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CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia

ABSTRACT: CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia

PROVIDER: PRJNA395514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5861500.fastq.gz	Fastqsanger.gz
	SRR5861501.fastq.gz	Fastqsanger.gz
	SRR5861502.fastq.gz	Fastqsanger.gz
	SRR5861512_1.fastq.gz	Fastqsanger.gz
	SRR5861512_2.fastq.gz	Fastqsanger.gz

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CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia [5C]

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CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia [5C]

Project description:We demonstrate that CBFb-SMMHCmaintains leukemia viability by inhibiting RUNX1 repression of MYC expression. Upon pharmacologic inhibition of CBF-SMMHC/RUNX1 binding, RUNX1 increases its association with three MYC distal downstream enhancers and represses MYC expression.

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Project description:We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFβ-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the transcriptional changes associated with AI-10-49, we performed RNA-seq analysis in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49.

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CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia [ATAC-seq]

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CBFb-SMMHC inhibition triggers apoptosis by disrupting MYC chromatin dynamics in acute myeloid leukemia [ChIP-seq]

Project description:We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFβ-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the epigenetic changes as well as RUNX1 binding associated with AI-10-49, we performed genome wide analysis of H3K27ac histone mark as well as RUNX1 bindings in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49.

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CHD7 deficiency delays leukemogenesis in mice induced by CBFB-MYH11

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