ArticleJournal for immunotherapy of cancer2026
Influence of USP15 and its derived-peptide on non-small cell lung cancer immune evasion via regulating PD-L1 stability.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- USP15 regulates mitotic fidelity, metastatic potential, and chemotherapeutic response in ovarian cancer cells.Molecular therapy. Oncology · 2026Article
- The role of USP19 in human diseases: from molecular function to clinical relevance.Frontiers in immunology · 2026Review
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Authors and funding
14 authors.
Funding
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Abstract
backgroundImmune checkpoint inhibitors (ICIs) therapy targeting programmed cell death protein 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) shows promising clinical benefits in non-small cell lung cancer (NSCLC). However, the relatively low response rate highlights the need to elucidate the regulatory mechanism of PD-L1 expression, and develop an alternative strategy to target PD-1/PD-L1 immune checkpoint pathway. Our study focuses on the role and mechanism of ubiquitin-specific protease 15 (USP15) and its derived peptide U10 on NSCLC immune evasion.
methodsUSP15 as PD-L1's deubiquitinase was identified by screening a human USP complementary DNA (cDNA) library. The role and mechanism of USP15 and its derived peptide U10 on PD-L1 stability in NSCLC cells were analyzed. T cell-mediated tumor cell killing activity and a syngeneic mouse NSCLC model were used to assess the influence of USP15 and U10 on NSCLC immune evasion. The antitumor effect of U10 in combination with PD-1 monoclonal antibody (mAb) via suppressing NSCLC immune evasion was also evaluated in mice. The expression and clinicopathological significance of USP15 and PD-L1 in cancer tissues were evaluated by immunohistochemistry.
resultsWe identify USP15 as a novel deubiquitinase of PD-L1. Mechanistically, USP15 binds and stabilizes PD-L1 in NSCLC cells by inhibiting its ubiquitination and degradation. Functionally, USP15 inhibits T cell ability of killing NSCLC cells in vitro, and promotes NSCLC immune evasion in mice via decreasing the population and activation of CD8
conclusionOur findings reveal a critical role for USP15 in PD-L1 stability regulation and NSCLC immune escape and develop a novel peptide as an alternative strategy for ICIs therapy of NSCLC.
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