ArticleOncogene2025
The deubiquitinase OTUD1 orchestrates cisplatin chemosensitivity of non-small cell lung cancer through destabilizing RAD23B/XPC.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Effect of xeroderma pigmentosum group C on the characteristics and regulatory mechanisms of lung cancer stem cells.International journal of oncology · 2026Article
- OTU deubiquitinases as immune-circuit editors: from human immunopathology to therapeutic prioritization.Frontiers in immunology · 2026Review
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Lung cancer, especially the subgroup non-small cell lung cancer (NSCLC), continues to be one of the most commonly diagnosed cancers and the leading cause of cancer-related deaths worldwide. Cisplatin has long been a cornerstone of chemotherapy and has improved the prognosis for NSCLC patients. However, its overall efficacy remains unsatisfactory, and patients ultimately develop drug resistance. Uncovering the underlying mechanism and identifying potential target to enhance cisplatin chemosensitivity is urgent. In this study, we uncovered that OTU deubiquitinase 1 (OTUD1) plays an important role in orchestrating cisplatin chemosensitivity of NSCLC. We found that promoter methylation resulted in downregulation of OTUD1 and the downregulated OTUD1 significantly associates with cisplatin resistance and poor prognosis in NSCLC. Overexpression of OTUD1 enhances cisplatin sensitivity in vitro and in vivo. Mechanistically, OTUD1 promoted the degradation of RAD23B-XPC complex, which is the critical factor for nucleotide excision repair to remove cisplatin-induced DNA adducts, leading to cisplatin-induced cell death. OTUD1 cleaves the K63-linked ubiquitin chain of RAD23B and XPC, and enhances PRKN mediated K48-linked ubiquitination of RAD23B-XPC and the subsequent proteasomal degradation. The findings of this study highlighted that OTUD1 could be a potential therapeutic target for NSCLC.
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Registered trials
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