ArticleScientific reports2020
STAT5-dependent regulation of CDC25A by miR-16 controls proliferation and differentiation in FLT3-ITD acute myeloid leukemia.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Novel CDK-independent function of CDC25 phosphatases in mRNA translation.EMBO reports · 2026Article
- Review
- ARRB2 promotes cervical cancer progression via stabilizing CDC25A mRNA through m6A-IGF2BP1-dependent manner.NPJ precision oncology · 2025Article
- Age-associated myeloid malignancies - the role of STAT3 and STAT5 in myelodysplastic syndrome and acute myeloid leukemia.FEBS letters · 2024Review
- Exploring the interplay between microRNA expression and DNA mutation analysis in AML patients.Saudi journal of biological sciences · 2024Article
- JAK/STAT in leukemia: a clinical update.Molecular cancer · 2024Review
- How ITD Insertion Sites Orchestrate the Biology and Disease of FLT3-ITD-Mutated Acute Myeloid Leukemia.Cancers · 2023Review
- Regulation of proton partitioning in kinase-activating acute myeloid leukemia and its therapeutic implication.Leukemia · 2022Article
- JAK-STAT in Early Hematopoiesis and Leukemia.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently identified the CDC25A phosphatase as a key actor in proliferation and differentiation in acute myeloid leukemia expressing the FLT3-ITD mutation. In this paper we demonstrate that CDC25A level is controlled by a complex STAT5/miR-16 transcription and translation pathway working downstream of this receptor. First, we established by CHIP analysis that STAT5 is directly involved in FLT3-ITD-dependent CDC25A gene transcription. In addition, we determined that miR-16 expression is repressed by FLT3-ITD activity, and that STAT5 participates in this repression. In accordance with these results, miR-16 expression was significantly reduced in a panel of AML primary samples carrying the FLT3-ITD mutation when compared with FLT3wt cells. The expression of a miR-16 mimic reduced CDC25A protein and mRNA levels, and RNA interference-mediated down modulation of miR-16 restored CDC25A expression in response to FLT3-ITD inhibition. Finally, decreasing miR-16 expression partially restored the proliferation of cells treated with the FLT3 inhibitor AC220, while the expression of miR-16 mimic stopped this proliferation and induced monocytic differentiation of AML cells. In summary, we identified a FLT3-ITD/STAT5/miR-16/CDC25A axis essential for AML cell proliferation and differentiation.
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