ArticleBlood cancer journal2020
A new regulatory mechanism of protein phosphatase 2A activity via SET in acute myeloid leukemia.
Article in Blood cancer journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Zebrafish tumor xenograft models for drug-screening: a systematic review of methods for treatment assessment.Journal of translational medicine · 2026Pooled it
- Advances in targeting p38 MAPK for cancer therapy: insights from molecular pharmacology and medicinal chemistry.Molecular diversity · 2026Review
- Greatwall kinase regulates acute myeloid leukaemia cell division through a non-canonical mechanism.EMBO reports · 2026Article
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- The Molecular Chaperone TCP1 Affects Carcinogenicity and Is a Potential Therapeutic Target for Acute Myeloid Leukemia.Pharmaceutics · 2025Article
- SET facilitates immune escape of microsatellite stability colorectal cancer by inhibiting c-Myc degradation.Cancer science · 2025Article
- Novel kinase regulators of extracellular matrix internalisation identified by high-content screening modulate invasive carcinoma cell migration.PLoS biology · 2024Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- Article
- Oncoprotein SET dynamically regulates cellular stress response through nucleocytoplasmic transport in breast cancer.Cell biology and toxicology · 2023Article
- Review
- DNA-PKcs as an upstream mediator of OCT4-induced MYC activation in small cell lung cancer.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Article
- Set Protein Is Involved in FLT3 Membrane Trafficking.Cancers · 2023Article
- Thirty years of SET/TAF1β/I2PP2A: from the identification of the biological functions to its implications in cancer and Alzheimer's disease.Bioscience reports · 2022Review
- SET/PP2A signaling regulates macrophage positioning in hypoxic tumor regions by amplifying chemotactic responses.Experimental & molecular medicine · 2022Article
- The E3 Ligase TRIM4 Facilitates SET Ubiquitin-Mediated Degradation to Enhance ER-α Action in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Article
- 4,5,7-Trisubstituted indeno[1,2-b]indole inhibits CK2 activity in tumor cells equivalent to CX-4945 and shows strong anti-migratory effects.FEBS open bio · 2022Article
- Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- CK2 Regulation: Perspectives in 2021.Biomedicines · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy. Although novel emerging drugs are available, the overall prognosis remains poor and new therapeutic approaches are required. PP2A phosphatase is a key regulator of cell homeostasis and is recurrently inactivated in AML. The anticancer activity of several PP2A-activating drugs (e.g., FTY720) depends on their interaction with the SET oncoprotein, an endogenous PP2A inhibitor that is overexpressed in 30% of AML cases. Elucidation of SET regulatory mechanisms may therefore provide novel targeted therapies for SET-overexpressing AMLs. Here, we show that upregulation of protein kinase p38β is a common event in AML. We provide evidence that p38β potentiates SET-mediated PP2A inactivation by two mechanisms: facilitating SET cytoplasmic translocation through CK2 phosphorylation, and directly binding to and stabilizing the SET protein. We demonstrate the importance of this new regulatory mechanism in primary AML cells from patients and in zebrafish xenograft models. Accordingly, combination of the CK2 inhibitor CX-4945, which retains SET in the nucleus, and FTY720, which disrupts the SET-PP2A binding in the cytoplasm, significantly reduces the viability and migration of AML cells. In conclusion, we show that the p38β/CK2/SET axis represents a new potential therapeutic pathway in AML patients with SET-dependent PP2A inactivation.
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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.