^
    Contact us  to learn more about
    our Premium Content:  News alerts, weekly reports and conference planners
    GENE:

    USP32 (Ubiquitin Specific Peptidase 32)

    i
    Other names: USP32, Ubiquitin Specific Peptidase 32, USP10, NY-REN-60, Ubiquitin-Specific-Processing Protease 32, Ubiquitin Carboxyl-Terminal Hydrolase 32, Renal Carcinoma Antigen NY-REN-60, Ubiquitin Specific Protease 32, Deubiquitinating Enzyme 32, Ubiquitin Thioesterase 32, Ubiquitin Thiolesterase 32
    Associations

    News

    Trials
    25d
    ResiDUBs: A deubiquitinating enzyme-based prognostic model identifies UBXN1 driving sorafenib resistance in liver cancer. (PubMed, Int Immunopharmacol)
    In vivo experiments further demonstrate that UBXN1 knockdown enhances the sensitivity of liver cancer cells to sorafenib and significantly reduces PI3K/AKT pathway activity. Our findings suggest that targeting UBXN1 may represent a promising therapeutic strategy to overcome sorafenib resistance in liver cancer.
    Journal
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    |
    sorafenib
    3ms
    Single-cell RNA sequence analysis reveals USP32 as a therapeutic target to mitigate PD-L1-driven colorectal tumorigenesis in vitro and in vivo. (PubMed, Theranostics)
    A combination of scRNA-seq analysis and wet-lab experimental validation confirmed that USP32 mediates PD-L1 protein stabilization in colon cancer, identifying it as a potential therapeutic target for CRC. CRISPR/Cas9-mediated targeted knockout of the USP32 gene reduced PD-L1 protein levels and significantly mitigated colorectal cell proliferation and tumorigenesis, both in vitro and in vivo, in a xenograft mouse model, underscoring a novel and alternative approach to the treatment of CRC.
    Preclinical • Journal • PD(L)-1 Biomarker • IO biomarker
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    |
    PD-L1 expression
    6ms
    USP32 stabilizes SEMA4C to promote malignant behavior of colon cancer cells. (PubMed, Pathol Res Pract)
    Overexpressing SEMA4C strengthened the weakened malignant behaviors of USP32-deficient CRC cells. These results indicate that USP32 acts as an oncogene in CRC by stabilizing SEMA4C, highlighting a new mechanism in CRC pathogenesis and suggesting USP32 as a novel potential therapeutic target for CRC treatment.
    Journal
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    9ms
    Phosphorylation of USP32 by CDK5 regulates Rap1 stability and therapeutic resistance in pancreatic ductal adenocarcinoma. (PubMed, Oncogene)
    Gemcitabine-based chemotherapy remains the cornerstone for advanced PDAC...Additionally, these functions can be significantly inhibited by pharmacological inhibition (roscovitine) or genetic ablation of CDK5...Increased expression of CDK5, USP32, and Rap1 is significantly associated with poorer prognosis in PDAC. We identified the previously unrecognized oncogenic function and clinical importance of the CDK5-USP32-Rap1 axis, providing preclinical evidence for potential new combination strategies for PDAC therapy.
    Journal
    |
    CDK5 (Cyclin Dependent Kinase 5) • USP32 (Ubiquitin Specific Peptidase 32)
    |
    gemcitabine • seliciclib (CYC202)
    11ms
    Lycobetaine Has Therapeutic Efficacy in Lung Squamous Cell Carcinoma by Targeting USP32 to Trigger Ferroptosis. (PubMed, Curr Issues Mol Biol)
    In orthotopic LUSC xenografts, the administration of LBT significantly inhibited tumor growth and metastasis and induced ferroptosis by targeting the USP32-NRF2 signaling axis. Taken together, these data suggest that LBT exerts its anticancer effects by inhibiting USP32-mediated NRF2 deubiquitination to induce ferroptosis and that LBT may serve as a prospective USP32-targeting agent for LUSC treatment.
    Journal
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    11ms
    USP32 Promotes Colorectal Carcinoma Progression Through Activating NF-κB Signalling Pathway. (PubMed, J Cell Mol Med)
    Wet experiments also confirmed that USP32 is critical for the proliferation, survival, and migration of CRC cells and tumour growth, which may be due to the activation of the NF-κB signalling pathway. In conclusion, targeting the USP32-NF-κB axis may be a novel treatment strategy for CRC patients.
    Journal
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    over1year
    Genomic analysis reveals molecular characterization of CD30+ and CD30- extranodal natural killer/T-cell lymphomas (ENKTLs). (PubMed, Hum Pathol)
    Immunohistochemical analysis revealed that the expression pattern of BCL10 in normal lymphoid tissues was similar to that of BCL2; however, its expression in ENKTL cells was significantly higher (67.92% vs. 16.98%), implying the potential application of BCL10 inhibitors for treating ENKTLs. These results provide new insights into the genetic characteristics of CD30+ and CD30- ENKTLs, and could facilitate the clinical development of novel therapies for ENKTL.
    Journal • IO biomarker
    |
    BCL2 (B-cell CLL/lymphoma 2) • TNFRSF8 (TNF Receptor Superfamily Member 8) • CCND3 (Cyclin D3) • KDM5A (Lysine Demethylase 5A) • MUC6 (Mucin 6) • SERPINA9 (Serpin Family A Member 9) • USP32 (Ubiquitin Specific Peptidase 32) • USP7 (Ubiquitin Specific Peptidase 7)
    over1year
    USP32 facilitates non-small cell lung cancer progression via deubiquitinating BAG3 and activating RAF-MEK-ERK signaling pathway. (PubMed, Oncogenesis)
    Furthermore, USP32 increased the phosphorylation level of the RAF/MEK/ERK signaling pathway in NSCLC cells by stabilizing BAG3. In summary, these findings imply that USP32 is critical to the development of NSCLC and could offer a theoretical framework for the clinical diagnosis and management of NSCLC patients in the future.
    Journal • IO biomarker
    |
    BCL2 (B-cell CLL/lymphoma 2) • BAG1 (BAG Cochaperone 1) • USP32 (Ubiquitin Specific Peptidase 32)
    2years
    Characterization and proposed therapeutic exploitation of fusion RNAs in metastatic breast cancers (YIR 2024)
    Taken together, these results demonstrate that fusion RNAs in MBC—some recurrent, many highly expressed and unique to individual tumors—are common. We create the most comprehensive catalog of ESR1 fusions in MBC, better define their frequency, discover their enrichment in LumB-like tumors, and will discuss clinicopathologic and transcriptomic features associated with ESR1 fusion positive disease. We identify druggable fusions that would likely be missed by current testing standards, find recurrent loss-of-function fusion RNAs, and show that over one-third of metastatic cases harbor at least one outlier expressed fusion—many of which involve BrCarelated genes.
    BRCA Biomarker • Metastases
    |
    HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • ER (Estrogen receptor) • BRCA1 (Breast cancer 1, early onset) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • NF1 (Neurofibromin 1) • CDH1 (Cadherin 1) • CREBBP (CREB binding protein) • ARID1B (AT-Rich Interaction Domain 1B) • FOXP1 (Forkhead Box P1) • RPS6KB1 (Ribosomal Protein S6 Kinase B1) • TGFB1 (Transforming Growth Factor Beta 1) • AXIN1 (Axin 1) • MSI2 (Musashi RNA Binding Protein 2) • NEK11 (NIMA Related Kinase 11) • PRKCA (Protein Kinase C Alpha) • PIK3R3 (Phosphoinositide-3-Kinase Regulatory Subunit 3) • USP32 (Ubiquitin Specific Peptidase 32)
    |
    FGFR2 fusion • BRCA mutation • CDH1 expression
    |
    Prosigna™ Breast Cancer Prognostic Gene Signature Assay
    over2years
    High USP32 expression contributes to cancer progression and is correlated with immune infiltrates in hepatocellular carcinoma. (PubMed, BMC Cancer)
    USP32 is highly expressed in HCC and closely correlates with the TME of HCC. It is a potential target for improving the efficacy of chemotherapy and developing new strategies for targeted therapy and immunotherapy in HCC.
    Journal • IO biomarker
    |
    USP32 (Ubiquitin Specific Peptidase 32)
    over2years
    Targeting MET endocytosis or degradation to overcome HGF-induced gefitinib resistance in EGFR-sensitive mutant lung adenocarcinoma. (PubMed, Biochem Biophys Res Commun)
    Additionally, we demonstrated that promoting MET degradation through deubiquitinase (USP8 or USP32) gene silence is another effective method for reversing drug resistance. Overall, our findings suggest that targeting MET receptor endocytosis and degradation is an attractive strategy for overcoming HGF-induced gefitinib resistance in EGFR-sensitive mutant lung adenocarcinoma.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • GRB2 (Growth Factor Receptor Bound Protein 2) • USP32 (Ubiquitin Specific Peptidase 32)
    |
    EGFR mutation
    |
    gefitinib
    over2years
    USP32 deubiquitinase: cellular functions, regulatory mechanisms, and potential as a cancer therapy target. (PubMed, Cell Death Discov)
    The therapeutic importance of USP32 in cancer treatment remains to be further proven. In conclusion, there are many options for the future direction of USP32 research.
    Review • Journal
    |
    USP32 (Ubiquitin Specific Peptidase 32)