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Mus musculus

ABSTRACT: Chromatin state changes in HOXA9/MEIS1 leukemia cells [4C-Seq]

PROVIDER: PRJNA401756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6003940.fastq.gz	Fastqsanger.gz
	SRR6003941.fastq.gz	Fastqsanger.gz
	SRR6003942.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Chromatin state changes in HOXA9/MEIS1 leukemia cells [ChIP-Seq]

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Project description:RNA expression changes in HOXA9/MEIS1 leukemia cells

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Hoxa9 and Meis1 cooperatively induce addiction to Syk signaling by suppressing miR-146a in acute myeloid leukemia

Project description:The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho)proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feed-forward loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU.1. In the context of Hoxa9 overexpression, Syk induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, we show that Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia.

2017-06-14 | PXD004192 | Pride

MicroRNA-155 is upregulated in Hoxa9/Meis1 leukemia inducing cells but is dispensable for in vivo transformation and leukemia development

Project description:OBJECTIVE: The microRNA miR-155 is upregulated in Hoxa9 and Meis1 leukemia inducing cells (LIC) , and miR-155 accelerates the onset of acute myeloid leukemia (AML) together with Hoxa9 but through largely unknown molecular mechanisms. The impact of miR-155 on accelerated onset of leukemia in the context of Hoxa9 and Meis1 is also unclear. To further resolve this, we performed a gene expression profiling, in the context of Hoxa9 and Meis1 leukemogenesis with miR-155 knocked out. RESULTS: Gene expression profiling of Hoxa9/Meis1 LIC without miR-155 does not delay the onset of AML and the gene expression changes are small

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Project description:Effect of loss of Jmjd1c on Hoxa9/Meis1 leukemia

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Effect of loss of Jmjd1c on Hoxa9/Meis1 leukemia

Project description:Analysis of gene expression profile of Hoxa9/Meis1 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and Hoxa9/Meis1 leukemia cells. These results provide insight into the role of Jmjd1c in AML with elelvated expression of Hoxa9.

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Project description:The role of Hoxa9 and Meis1 in development of acute myeloid leukemia

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miRNAs differentially expressed in MLL-AF9-transduced versus HOXA9/MEIS1-transduced LSK cells

Project description:HOXA9 and MEIS1 are essential downstream effectors of the MLL-AF9 oncoprotein during leukemia induction. Leukemia derived from MLL-AF9-transduced LSK cells has a more aggressive phenotype than that derived from HOXA9/MEIS1-transduced LSK cells. To determine differential miRNA expression that contributes to increased aggressiveness in MLL-AF9-induced leukemia, miRCURY LNA microRNA Array was performed on LSK cells transduced with MLL-AF9 versus HOXA/MEIS1 oncogenes.

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Project description:Gene expression profiles upon Meis1 knockout in Hoxa9/Meis1-induced AML

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Project description:The role of Hoxa9 and Meis1 in development of acute myeloid leukemia (mRNA)

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