ArticleBMC cancer2025
Oncogenic and immunological functions of USP35 in pan-cancer and its potential as a biomarker in kidney clear cell carcinoma.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Multi-omics characterization identifies AHCY as a prognostic biomarker driving immunometabolic reprogramming in bladder cancer.Translational oncology · 2026Article
- Regulatory roles of five key USP family deubiquitinases in cancer: from mechanisms to targeted therapy advances.Frontiers in pharmacology · 2026Review
- The deubiquitinase USP35: from an oncogenic hub to a therapeutic target in human cancers.Frontiers in oncology · 2026Review
- Roles of E3 ubiquitin ligases and deubiquitinating enzymes in renal cell carcinoma.Frontiers in oncology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundUbiquitin-specific protease 35 (USP35) has gained attention as a regulator in cancer progression. However, its specific role in kidney clear cell carcinoma (KIRC) remains unclear.
methodsUSP35 expression in KIRC tumor and normal tissues was evaluated using TCGA data. Correlations between USP35 expression, clinical parameters, and survival outcomes were examined. Functional enrichment analyses were performed to explore the pathways associated with USP35 expression. Immune-related analyses were conducted to assess the effect of USP35 on immune cell recruitment and neoantigen presentation. Drug sensitivity analyses were used to identify potential therapeutic agents targeting USP35.
resultsUSP35 was significantly overexpressed in KIRC tumor tissues compared to normal tissues, and its high expression correlated with advanced disease stages and poor survival outcomes. Gene set enrichment analysis revealed that high USP35 expression was associated with oncogenic pathways, including glycerophospholipid and linoleic acid metabolism, while low expression linked to nitrogen and purine metabolism. USP35 also modulated immune responses, affecting immune cell recruitment and neoantigen presentation, suggesting a role in immune evasion. Drug sensitivity analysis showed that high USP35 expression correlated with increased sensitivity to paclitaxel, bosutinib, and lapatinib. In vitro knockdown of USP35 significantly reduced KIRC cell proliferation, migration, and epithelial-mesenchymal transition (EMT), further supporting its role in tumor progression.
conclusionUSP35 is overexpressed in KIRC and associated with poor prognosis, likely promoting tumor progression through oncogenic pathways and immune modulation. Its correlation with drug sensitivity positions USP35 as a potential therapeutic target, warranting further investigation into its mechanistic functions and therapeutic applications.
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