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PSPC1 selectively controls tumorigenesis and oncogenic transcription in acute myeloid leukemia [ChIP-seq]

GSE247300 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 5 samples Submitted 2025/05/30 Platform GPL24676
Summary
Acute myeloid leukemia (AML) is an aggressive hematopoietic malignancy characterized by the blockage of myeloid cell differentiation and uncontrolled proliferation of immature myeloid cells. Here, we show that paraspeckle component 1 (PSPC1) is aberrantly overexpressed in AML and high level of PSPC1 expression is associated with poor survival in AML patients. We demonstrate that PSPC1 loss dramatically suppresses leukemia maintenance and initiation/development as well as self-renewal of leukemia stem cells (LSCs) but has no effect on normal hematopoiesis. Mechanistically, PSPC1 interacts with PU.1, and they co-occupy the chromatin, especially at promoter regions proximal to transcription start site (TSS). Recruitment of PSPC1 and PU.1 on co-bound regions was dependent on each other to regulate target genes expression such as NDC1, a prognostic marker in multiple tumors. Collectively, our findings uncover a selective and crucial role of PSPC1 in AML and highlight its potential as a promising therapeutic target for myeloid malignancies.
Published in
PSPC1 exerts an oncogenic role in AML by regulating a leukemic transcription program in cooperation with PU.1
Hong J, Sui P, Li Y et al. · Cell stem cell 2025 · PMID 39954676 · doi:10.1016/j.stem.2025.01.010
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Also filed as BioProject PRJNA1037083 and SRA study SRP470830. Searching any of these in the dataset finder brings you back here.

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