ArticleBlood2023
PRL2 phosphatase enhances oncogenic FLT3 signaling via dephosphorylation of the E3 ubiquitin ligase CBL at tyrosine 371.
Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular and clinical analyses of c-CBL mutations affecting tyrosine 371 in myelodysplastic and proliferative disorders.Leukemia · 2026Article
- Phosphatases of regenerating liver downregulate PTEN to promote tumorigenesis.Biochemical Society transactions · 2026Review
- PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.Blood advances · 2026Article
- Single-cell transcriptomics uncover RNF130-mediated TNF-α pathway activation and worenine synergy with paclitaxel in breast cancer.Clinical epigenetics · 2026Article
- Metabolic reprogramming and immune regulation in acute myeloid leukemia.Frontiers in immunology · 2025Review
- GPSD: a hybrid learning framework for the prediction of phosphatase-specific dephosphorylation sites.Briefings in bioinformatics · 2024Article
- The roles of ubiquitination in AML.Annals of hematology · 2024Review
- PTP4A2 Promotes Glioblastoma Progression and Macrophage Polarization under Microenvironmental Pressure.Cancer research communications · 2024Article
- Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024Review
- PRL2 Phosphatase Promotes Oncogenic KIT Signaling in Leukemia Cells through Modulating CBL Phosphorylation.Molecular cancer research : MCR · 2024Article
- Inhibition of PRL2 Upregulates PTEN and Attenuates Tumor Growth in Tp53-deficient Sarcoma and Lymphoma Mouse Models.Cancer research communications · 2024Article
- PRL2 inhibition elevates PTEN protein and ameliorates progression of acute myeloid leukemia.JCI insight · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
26 authors at 7 institutions in 3 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is an aggressive blood cancer with poor prognosis. FMS-like tyrosine kinase receptor-3 (FLT3) is one of the major oncogenic receptor tyrosine kinases aberrantly activated in AML. Although protein tyrosine phosphatase PRL2 is highly expressed in some subtypes of AML compared with normal human hematopoietic stem and progenitor cells, the mechanisms by which PRL2 promotes leukemogenesis are largely unknown. We discovered that genetic and pharmacological inhibition of PRL2 significantly reduce the burden of FLT3-internal tandem duplications-driven leukemia and extend the survival of leukemic mice. Furthermore, we found that PRL2 enhances oncogenic FLT3 signaling in leukemia cells, promoting their proliferation and survival. Mechanistically, PRL2 dephosphorylates the E3 ubiquitin ligase CBL at tyrosine 371 and attenuates CBL-mediated ubiquitination and degradation of FLT3, leading to enhanced FLT3 signaling in leukemia cells. Thus, our study reveals that PRL2 enhances oncogenic FLT3 signaling in leukemia cells through dephosphorylation of CBL and will likely establish PRL2 as a novel druggable target for AML.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.