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Effect of NOX2 (CYBB) knock out on the transcriptome of leukemia stem cells isolated from NUP98/HOXA9+BCR/ABL murine syngeneic leukemia model

ABSTRACT: Effect of NOX2 (CYBB) knock out on the transcriptome of leukemia stem cells isolated from NUP98/HOXA9+BCR/ABL murine syngeneic leukemia model

PROVIDER: PRJNA482839 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7591874.fastq.gz	Fastqsanger.gz
	SRR7591875.fastq.gz	Fastqsanger.gz
	SRR7591876.fastq.gz	Fastqsanger.gz
	SRR7591877.fastq.gz	Fastqsanger.gz

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Effect of NOX2 (CYBB) knock out on the transcriptome of leukemia stem cells isolated from NUP98/HOXA9+BCR/ABL murine syngeneic leukemia model

Project description:To investigate the function of NOX2 (CYBB) in leukemia stem cells, we created leukemia by tranforming primitive hematopoetic cells isolated from wild type and NOX2-KO mice with NUP98/HOXA9 and BCR/ABL oncogenes, isolated mRNA, and performed RNA-seq experiments to profile transcriptional changes upon NOX2 loss.

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Expression data from murine hematopoietic cells expressing BCR-ABL alone, NUP98-HOXA9 alone, BCR-ABL and NUP98-HOXA9, or null for both oncogenes

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Project description:Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. Molecular analyses indicate that MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.

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