ArticleLeukemia2016
UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- Pharmacological inhibition of UBASH3B induces mitotic arrest and selectively reduces tumor growth.EMBO molecular medicine · 2026Article
- MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2.Leukemia · 2026Article
- Investigating the role of UBASH3B in cancer: structural relevance, physiological functions, and therapeutic possibilities.Journal of experimental & clinical cancer research : CR · 2025Review
- Innate immune cell barrier-related genes inform precision prognosis in pancreatic cancer.Frontiers in immunology · 2025Article
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- Modeling and therapeutic targeting of t(8;21) AML with/without TP53 deficiency.International journal of hematology · 2024Article
- Role of Tula-Family Proteins in Cell Signaling and Activation: Advances and Challenges.International journal of molecular sciences · 2024Article
- FLI1 induces erythroleukemia through opposing effects on UBASH3A and UBASH3B expression.BMC cancer · 2024Article
- Integrative analysis of cancer multimodality data identifying COPS5 as a novel biomarker of diffuse large B-cell lymphoma.Frontiers in genetics · 2024Article
- Review
- Hyperactive Natural Killer cells in Rag2 knockout mice inhibit the development of acute myeloid leukemia.Communications biology · 2023Article
- TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023Review
- IMPDH inhibition activates TLR-VCAM1 pathway and suppresses the development of MLL-fusion leukemia.EMBO molecular medicine · 2023Article
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- Non-proteolytic ubiquitylation in cellular signaling and human disease.Communications biology · 2022Review
- Converging genetic and epigenetic drivers of paediatric acute lymphoblastic leukaemia identified by an information-theoretic analysis.Nature biomedical engineering · 2021Article
- Review
- Article
- Phospho-PTM proteomic discovery of novel EPO- modulated kinases and phosphatases, including PTPN18 as a positive regulator of EPOR/JAK2 Signaling.Cellular signalling · 2020Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
The t(8;21) rearrangement, which creates the AML1-ETO fusion protein, represents the most common chromosomal translocation in acute myeloid leukemia (AML). Clinical data suggest that CBL mutations are a frequent event in t(8;21) AML, but the role of CBL in AML1-ETO-induced leukemia has not been investigated. In this study, we demonstrate that CBL mutations collaborate with AML1-ETO to expand human CD34+ cells both in vitro and in a xenograft model. CBL depletion by shRNA also promotes the growth of AML1-ETO cells, demonstrating the inhibitory function of endogenous CBL in t(8;21) AML. Mechanistically, loss of CBL function confers hyper-responsiveness to thrombopoietin and enhances STAT5/AKT/ERK/Src signaling in AML1-ETO cells. Interestingly, we found the protein tyrosine phosphatase UBASH3B/Sts-1, which is known to inhibit CBL function, is upregulated by AML1-ETO through transcriptional and miR-9-mediated regulation. UBASH3B/Sts-1 depletion induces an aberrant pattern of CBL phosphorylation and impairs proliferation in AML1-ETO cells. The growth inhibition caused by UBASH3B/Sts-1 depletion can be rescued by ectopic expression of CBL mutants, suggesting that UBASH3B/Sts-1 supports the growth of AML1-ETO cells partly through modulation of CBL function. Our study reveals a role of CBL in restricting myeloid proliferation of human AML1-ETO-induced leukemia, and identifies UBASH3B/Sts-1 as a potential target for pharmaceutical intervention.
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Registered trials
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.