ArticleProceedings of the National Academy of Sciences of the United States of America2013
Protein tyrosine phosphatase UBASH3B is overexpressed in triple-negative breast cancer and promotes invasion and metastasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- RASAL2 activates RAC1 to promote triple-negative breast cancer progression.The Journal of clinical investigation · 2014Trial
- Pharmacological inhibition of UBASH3B induces mitotic arrest and selectively reduces tumor growth.EMBO molecular medicine · 2026Article
- A novelBlood science (Baltimore, Md.) · 2026Article
- The role of disulfidptosis-driven tumor microenvironment remodeling in pancreatic cancer progression.Frontiers in immunology · 2026Article
- Investigating the role of UBASH3B in cancer: structural relevance, physiological functions, and therapeutic possibilities.Journal of experimental & clinical cancer research : CR · 2025Review
- LncRNA NRAD1 regulates the triple-negative breast cancer transcriptome by miRNA biogenesis, localization, and predominately non-ceRNA interactions.Scientific reports · 2025Article
- Innate immune cell barrier-related genes inform precision prognosis in pancreatic cancer.Frontiers in immunology · 2025Article
- Topological Data Analysis Reveals a Subgroup of Luminal B Breast Cancer.IEEE open journal of engineering in medicine and biology · 2025Article
- Baicalein inhibits cell proliferation and induces apoptosis in brain glioma cells by downregulating the LGR4-EGFR pathway.Cancer gene therapy · 2024Article
- UBASH3B-mediated MRPL12 Y60 dephosphorylation inhibits LUAD development by driving mitochondrial metabolism reprogramming.Journal of experimental & clinical cancer research : CR · 2024Article
- Role of Tula-Family Proteins in Cell Signaling and Activation: Advances and Challenges.International journal of molecular sciences · 2024Article
- Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease.Clinical and experimental immunology · 2024Article
- FLI1 induces erythroleukemia through opposing effects on UBASH3A and UBASH3B expression.BMC cancer · 2024Article
- TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023Review
- Non-proteolytic ubiquitylation in cellular signaling and human disease.Communications biology · 2022Review
- Genetic variation influencing DNA methylation provides insights into molecular mechanisms regulating genomic function.Nature genetics · 2022Article
- The third international hackathon for applying insights into large-scale genomic composition to use cases in a wide range of organisms.F1000Research · 2022Article
- The Anticancer Effects of Flavonoids through miRNAs Modulations in Triple-Negative Breast Cancer.Nutrients · 2021Review
- Identification of novel prognostic genes of triple-negative breast cancer using meta-analysis and weighted gene co-expressed network analysis.Annals of translational medicine · 2021Article
- Spatiotemporal profiling of cytosolic signaling complexes in living cells by selective proximity proteomics.Nature communications · 2021Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efforts to improve the clinical outcome of highly aggressive triple-negative breast cancer (TNBC) have been hindered by the lack of effective targeted therapies. Thus, it is important to identify the specific gene targets/pathways driving the invasive phenotype to develop more effective therapeutics. Here we show that ubiquitin-associated and SH3 domain-containing B (UBASH3B), a protein tyrosine phosphatase, is overexpressed in TNBC, where it supports malignant growth, invasion, and metastasis largely through modulating epidermal growth factor receptor (EGFR). We also show that UBASH3B is a functional target of anti-invasive microRNA200a (miR200a) that is down-regulated in TNBC. Importantly, the oncogenic potential of UBASH3B is dependent on its tyrosine phosphatase activity, which targets CBL ubiquitin ligase for dephosphorylation and inactivation, leading to EGFR up-regulation. Thus, UBASH3B may function as a crucial node in bridging multiple invasion-promoting pathways, thereby providing a potential therapeutic target for TNBC.
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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.