ArticleFrontiers in oncology2025
COP1 drives renal cell carcinoma progression by targeting ACSL4 for ubiquitin-mediated degradation and inhibiting ferroptosis.
Article in Frontiers in oncology, 2025. 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.
- Multi-omics analysis of patient-derived organoids reveals that E3 ligase COP1 promotes liver metastasis and oxaliplatin resistance in colorectal cancer through LUZP1 degradation and MYL9 phosphorylation.Experimental hematology & oncology · 2026Article
- Ferroptosis in renal cell carcinoma: integrative multi-omics insights and therapeutic perspectives.International journal of surgery (London, England) · 2026Article
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Authors and funding
4 authors.
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Abstract
Background: Renal cell carcinoma (RCC) progression is closely linked to dysregulation of the ubiquitin-proteasome system, particularly aberrant ubiquitination processes governing protein degradation and cell cycle control. As a pivotal E3 ubiquitin ligase, COP1 mediates substrate-specific ubiquitination to regulate protein stability. However, its functional role in RCC remains poorly characterized. This study investigates how COP1 drives RCC malignancy and explores its underlying molecular mechanisms. Methods: We analyzed the expression of COP1 in RCC cells and its relationship with patient overall survival (OS) in databases. The CCK-8 assay was used to detect the effect of COP1 on the proliferation of RCC cells, while the Transwell assay was used to assess the impact of COP1 on the migration and invasion of RCC cells. We employed mass spectrometry, co-immunoprecipitation, Western blot, and RT-qPCR to explore the target proteins that interact with COP1 and their interaction modes. After inducing with ferroptosis inducers, we measured the effect of COP1 on lipid ROS levels in RCC cells. Finally, we validated the role of COP1 in RCC using Results: COP1 was significantly correlated with poor patient prognosis. Functional studies demonstrated that COP1 overexpression markedly increased RCC cell proliferation by 65% (786-O) and 58% (ACHN) ( Conclusion: Our study establishes COP1 as a critical driver of RCC progression by suppressing ferroptosis through ubiquitin-mediated degradation of ACSL4, thereby providing a novel theoretical foundation for targeted therapeutic strategies in RCC.
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