ArticleMolecular cancer2014
USP18 is crucial for IFN-γ-mediated inhibition of B16 melanoma tumorigenesis and antitumor immunity.
Article in Molecular cancer, 2014. 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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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Towards a transcriptomic biomarker for the classification of melanocytic neoplasms.PLoS genetics · 2025Article
- Targeting USP18 overcomes acquired resistance in hepatocellular carcinoma by regulating NCOA4 deISGylation and ferroptosis.Cell death & disease · 2025Article
- Dual role of interferon-gamma in the response of melanoma patients to immunotherapy with immune checkpoint inhibitors.Molecular cancer · 2025Review
- Regulatory T cells crosstalk with tumor cells and endothelium through lymphotoxin signaling.Nature communications · 2024Article
- Review
- USP18 Is Associated with PD-L1 Antitumor Immunity and Improved Prognosis in Colorectal Cancer.Biomolecules · 2024Article
- Ubiquitin modification in the regulation of tumor immunotherapy resistance mechanisms and potential therapeutic targets.Experimental hematology & oncology · 2024Review
- Bulk and single cells transcriptomes with experimental validation identify USP18 as a novel glioma prognosis and proliferation indicator.Experimental and therapeutic medicine · 2024Article
- Article
- Targeting ubiquitin specific proteases (USPs) in cancer immunotherapy: from basic research to preclinical application.Journal of experimental & clinical cancer research : CR · 2023Review
- High expression of USP18 is associated with the growth of colorectal carcinoma.Histology and histopathology · 2021Article
- Article
- USP18-deficiency in cervical carcinoma is crucial for the malignant behavior of tumor cells in an ERK signal-dependent manner.Oncology letters · 2021Article
- Single-Molecule RNA Sequencing Reveals IFNγ-Induced Differential Expression of Immune Escape Genes in Merkel Cell Polyomavirus-Positive MCC Cell Lines.Frontiers in microbiology · 2021Article
- Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020Review
- USP18 deubiquitinates and stabilizes Twist1 to promote epithelial-mesenchymal transition in glioblastoma cells.American journal of cancer research · 2020Article
- Upregulation of Enzymes involved in ISGylation and Ubiquitination in patients with hepatocellular carcinoma.International journal of medical sciences · 2020Article
- Abnormal expression of circulating and tumor-infiltrating carcinoembryonic antigen-related cell adhesion molecule 1 in patients with glioma.Oncology letters · 2018Article
- Evidence for the ISG15-Specific Deubiquitinase USP18 as an Antineoplastic Target.Cancer research · 2018Review
- Combined Blockade of T Cell Immunoglobulin and Mucin Domain 3 and Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Results in Durable Therapeutic Efficacy in Mice with Intracranial Gliomas.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundInterferon (IFN)-γ-mediated immune response plays an important role in tumor immunosurveillance. However, the regulation of IFN-γ-mediated tumorigenesis and immune response remains elusive. USP18, an interferon stimulating response element, regulates IFN-α-mediated signaling in anti-viral immune response, but its role in IFN-γ-mediated tumorigenesis and anti-tumor immune response is unknown.
methodIn this study, USP18 in tumorigenesis and anti-tumor immune response was comprehensively appraised in vivo by overexpression or downregulation its expression in murine B16 melanoma tumor model in immunocompetent and immunodeficient mice.
resultsEctopic expression or downregulation of USP18 in B16 melanoma tumor cells inhibited or promoted tumorigenesis, respectively, in immunocompetent mice. USP18 expression in B16 melanoma tumor cells regulated IFN-γ-mediated immunoediting, including upregulating MHC class-I expression, reducing tumor cell-mediated inhibition of T cell proliferation and activation, and suppressing PD-1 expression in CD4+ and CD8+ T cells in tumor-bearing mice. USP18 expression in B16 melanoma tumor cells also enhanced CTL activity during adoptive immunotherapy by prolonging the persistence and enhancing the activity of adoptively transferred CTLs and by reducing CTL exhaustion in the tumor microenvironment. Mechanistic studies demonstrated that USP18 suppressed tumor cell-mediated immune inhibition by activating T cells, inhibiting T-cell exhaustion, and reducing dendritic cell tolerance, thus sensitizing tumor cells to immunosurveillance and immunotherapy.
conclusionThese findings suggest that stimulating USP18 is a feasible approach to induce B16 melanoma specific immune response.
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