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Expression profile of small nucleolar RNA (snoRNA) in acute myeloid leukemia.

ABSTRACT: Expression profile of small nucleolar RNA (snoRNA) in acute myeloid leukemia.

OTHER RELATED OMICS DATASETS IN: GSE80602GSE80523

PROVIDER: PRJNA319190 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3407260.fastq.gz	Fastqsanger.gz
	SRR3407270.fastq.gz	Fastqsanger.gz
	SRR3407280.fastq.gz	Fastqsanger.gz
	SRR3407290.fastq.gz	Fastqsanger.gz
	SRR3407300.fastq.gz	Fastqsanger.gz

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Expression profile of small nucleolar RNA (snoRNA) in acute myeloid leukemia.

Project description:Leukemogenesis requires enhanced self-renewal activity, which is induced by specific oncogenes. The underlying molecular mechanisms remain incompletely understood. We transduced mouse lineage negative bone marrow cells (enriched for hematopoietic stem and progenitor cells) with retrovirus expressing leukemic oncogene AML1-ETO9a, MYC and MLL-AF9 as well as empty vector (MIG). We found that all three oncogenes enhanced snoRNA formation. High abundance of snoRNAs was observed in primary human AML specimens with the notable exception of NPM1 mutant AML. Leukemogenesis by AML1-ETO required expression of the groucho related Amino Enhancer of Split (AES). AES functioned by inducing snoRNA/RNP formation via interaction with the RNA helicase DDX21. Similarly, loss of C/D box snoRNAs with concomitant loss of rRNA 2’-O-methylation resulted in decreased leukemia self-renewal potential.In summary, we identified C/D box snoRNAs and rRNA 2’-O-methylation as critical determinants of leukemic stem cell activity.

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Project description:Acute myeloid leukemia (AML) is a disease with poor outcome but patients harbouring certain chromosomal rearrangements or complex karyotypes have particularly adverse prognosis. For these patients, targeted therapies have not yet made a significant clinical impact. To understand the molecular landscape of poor risk AML we profiled 55 poor risk AML patients using a multiomics approach that included transcriptomics (n=39), proteomics (n=55), phosphoproteomics (n=55) and an ex vivo drug sensitivity screening (482 compounds tested in at least 30 patients). We identified a phosphoproteomics signature that define two biologically distinct groups of KMT2A rearranged leukaemia, which we term MLLGA and MLLGB. MLLGA presented increased DOT1L phosphorylation, HOXA gene expression, CDK1 activity and phosphorylation of proteins involved in RNA metabolism, replication and DNA damage when compared to MLLGB and no KMT2A rearranged samples. MLLGA was particularly sensitive to 15 compounds including genotoxic drugs and inhibitors of mitotic kinases and IMPDH relative to other cases. The expression of IMPDH2 and multiple nucleolar proteins was higher in MLLGA and correlated with the response to IMPDH inhibition in KMT2A rearranged leukaemia, suggesting a role of the nucleolar activity in sensitivity to IMPDH inhibition. In summary, our multilayer molecular profiling of poor risk AML matched to the response to hundreds of compounds identified a phosphoproteomics signature that define two biologically and phenotypically distinct groups of KMT2A rearranged leukaemia. These data provide a rationale for the development of specific therapies for KMT2A subgroups characterised by the MLLGA phosphoproteomics signature identified in this study.

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