ArticleCell stem cell2025
PSPC1 exerts an oncogenic role in AML by regulating a leukemic transcription program in cooperation with PU.1.
Article in Cell stem cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Review
- Article
- EXOSC4 as a novel regulator of neddylation in acute myeloid leukemia.Scientific reports · 2026Article
- Development of PolyHis-Targeting PROTAC Degraders.Angewandte Chemie (International ed. in English) · 2026Article
- Dickkopf 2 serves as a novel therapeutic target and prognostic biomarker in acute myeloid leukemia targeted by evodiamine.Frontiers in medicine · 2026Article
- ZEB1 directly activates IL-6 to promote triple-negative breast cancer stemness in an epigenetically constrained context.Frontiers in oncology · 2026Article
- Paraspeckle component 1 in acute myeloid leukemia: prospects for therapeutic targeting.Expert opinion on therapeutic targets · 2026Article
- Integrative Bioinformatics Reveals Novel Molecular Mechanisms and Therapeutic Targets in Acute Myeloid Leukaemia.Journal of cellular and molecular medicine · 2026Article
- Review
- Paraspeckle Component 1: a multifunctional RNA binding protein.American journal of cancer research · 2025Review
- Liquid-liquid phase separation in gastric cancer: identifying novel biomarkers and therapeutic targets through gene signature analysis.Frontiers in immunology · 2025Article
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25 authors.
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Abstract
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 and associated with poor survival in AML patients. Using human AML cells and mouse models, we demonstrate that PSPC1 is not required for normal hematopoiesis, but it is critical and essential for AML cells to maintain their leukemic characteristics. PSPC1 loss induces robust differentiation, suppresses proliferation, and abolishes leukemogenesis in diverse AML cells. Mechanistically, PSPC1 exerts a pro-leukemia effect by regulating a unique leukemic transcription program via cooperative chromatin binding with PU.1 and activation of tumor-promoting genes, including NDC1, which is not previously implicated in AML. Our findings uncover a unique and crucial role of PSPC1 dependency in AML and highlight its potential as a promising therapeutic target for AML.
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