ArticleCell death & disease2024
USP3 promotes osteosarcoma progression via deubiquitinating EPHA2 and activating the PI3K/AKT signaling pathway.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- HILPDA, Regulated by WTAP in an m6A-Dependent Manner, Enhances Osteosarcoma Development by Inhibiting Ferroptosis and Promoting Glycolysis.Biochemical genetics · 2026Article
- Article
- Integrative bioinformatics, network toxicology, and molecular docking elucidate molecular mechanisms of ATBC-induced sarcoma progression with experimental validation.BMC pharmacology & toxicology · 2026Article
- RHBDL2 drives lipid metabolic reprogramming in osteosarcoma via USP3-mediated deubiquitination of PPT1.Cell death & disease · 2026Article
- Mechanism of RBM15 in the Immune Escape of Non-small Cell Lung Cancer Cells Via the LncRNA EGFR-AS1/USP3/PD-L1 Axis.Biological procedures online · 2026Article
- USP3 stabilizes MIC19 by deubiquitination under hypoxic stress and promotes the progression of non-small cell lung cancer.Acta pharmacologica Sinica · 2026Article
- MicroRNA-374b-5p suppresses osteosarcoma progression via the PDPK1-mediated AKT pathway.Translational cancer research · 2026Article
- Nanoparticles Targeting the Tumor Microenvironment for the Treatment of Osteosarcoma: Recent Progress and Perspectives.International journal of nanomedicine · 2026Review
- GPX8 is transcriptionally regulated by KLF16 and promotes osteosarcoma progression.Journal of translational medicine · 2025Article
- Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA.Annals of medicine · 2025Review
- Knockdown of CTMP Enhances Progesterone Sensitivity in Endometrial Cancer by Inhibiting the PI3K/AKT Signaling Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Dcaf15-mediated EphA2 degradation triggers disruption of the blood-brain barrier during Streptococcus suis meningitis.Communications biology · 2025Article
- HMGB1 and Its Signaling Pathway in Osteosarcoma: Current Advances in Targeted Therapy.Current issues in molecular biology · 2025Review
- TRIM47 Facilitates Osteosarcoma Progression via Destabilising FBP1 and Thus Activation of Wnt/β-Catenin Pathway.Journal of cellular and molecular medicine · 2025Article
- METTL5-mediated m6A modification of UBE3C promotes osteosarcoma progression by suppressing ferroptosis via inducing AHNAK ubiquitination.Journal of molecular histology · 2025Article
- A Dual Approach with Organoid and CRISPR Screening Reveals ERCC6 as a Determinant of Cisplatin Resistance in Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- S100 A16 promotes the progression of osteosarcoma by activating the PI3 K/AKT signaling pathway through ANXA2.Scientific reports · 2025Article
- Article
- Zmynd11 is essential for neurogenesis by coordinating H3K36me3 modification of Epha2 and PI3K signaling pathway.Cell & bioscience · 2025Article
- Deubiquitinase Genes as Prognostic Biomarkers in Osteosarcoma: Insights From Single-Cell Sequencing and Machine Learning-Based Prognostic Modeling.International journal of genomics · 2025Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Ubiquitin-specific protease 3 (USP3) plays an important role in the progression of various tumors. However, the role of USP3 in osteosarcoma (OS) remains poorly understood. The aim of this study was to explore the biological function of USP3 in OS and the underlying molecular mechanism. We found that OS had higher USP3 expression compared with that of normal bone tissue, and high expression of USP3 was associated with poor prognosis in patients with OS. Overexpression of USP3 significantly increased OS cell proliferation, migration, and invasion. Mechanistically, USP3 led to the activation of the PI3K/AKT signaling pathway in OS by binding to EPHA2 and then reducing its protein degradation. Notably, the truncation mutant USP3-F2 (159-520) interacted with EPHA2, and amino acid 203 was found to play an important role in this process. And knockdown of EPHA2 expression reversed the pro-tumour effects of USP3-upregulating. Thus, our study indicates the USP3/EPHA2 axis may be a novel potential target for OS treatment.
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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.