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Understanding Early Stage Myelodysplastic Syndrome Pathobiology

ABSTRACT: Understanding Early Stage Myelodysplastic Syndrome Pathobiology

PROVIDER: PRJNA476461 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7350960_1.fastq.gz	Fastqsanger.gz
	SRR7350960_2.fastq.gz	Fastqsanger.gz
	SRR7350970_1.fastq.gz	Fastqsanger.gz
	SRR7350970_2.fastq.gz	Fastqsanger.gz
	SRR7350980_1.fastq.gz	Fastqsanger.gz

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Understanding Early Stage Myelodysplastic Syndrome Pathobiology

Project description:Delineating key HSC regulators is of significant interest for informing the treatment of hematologic malignancy. While HSC activity is enhanced by overexpression of SKI, the transforming growth factor-beta (TGFβ) signaling antagonist corepressor, its requirement in HSC is unknown. Here we reveal a profound defect in Ski-/- HSC fitness but not specification. Transcriptionally, Ski-/- HSC exhibited striking upregulation of TGFb superfamily signaling and splicing alterations. As these are both common aspects of myelodysplastic-syndrome (MDS) pathobiology with prognostic value, we investigated the role of SKI in MDS. A SKI-correlated gene signature defines a subset of low-risk MDS patients with active TGFβ signaling and deregulated RNA splicing (e.g. CSF3R). The apparent paradox of Ski-/- HSC sharing molecular aspects of MDS with elevated SKI-mRNA is resolved by miR-21 targeting of SKI in MDS. We conclude that miR-21-mediated loss of SKI contributes to early stage MDS pathogenesis by activating TGFβ signaling and alternative splicing while hindering HSC fitness.

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