ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2025
USP14 targets FABP5-mediated ferroptosis to promote proliferation and cisplatin resistance of HNSCC.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- USP14 promotes head and neck squamous cell carcinoma progression via deubiquitinating and stabilizing CFL2.Future science OA · 2026Article
- FABP5 confers resistance to drug-induced ROS toxicity in cervical cancer cell lines by suppressing the PPARγ/CPT1A signaling pathway.Discover oncology · 2026Article
- Ubiquitin-Specific Protease 45 Inhibits Lung Adenocarcinoma Ferroptosis by Regulating Ubiquitination and Stability of Glutathione Peroxidase 4.Cancer medicine · 2026Article
- Ferroptosis and cuproptosis in head and neck squamous cell carcinoma: interconnected mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Exosomal FABP5 drives HCC progression via macrophage lipid metabolism and immune microenvironment remodeling.Frontiers in immunology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundHead and neck squamous cell carcinoma (HNSCC) ranks among the most lethal solid tumors in humans, with a five-year survival rate hovering around 50%. The limited understanding of its biological foundation has hindered the development of efficacious targeted therapeutics.
methodsTCGA database and immunohistochemistry were deployed to confirm the expression levels of ubiquitin specific protease 14 (USP14). CCK8 method was used to evaluate the influence of USP14 on cisplatin resistance. Further investigations into the role of USP14 were conducted through assessments of cell proliferation, colony formation, and Transwell assays. The impact of USP14 expression on ferroptosis was evaluated by measuring GSH/GSSG ratios, Fe
resultsOur analysis revealed that USP14 ranked among the most prominently upregulated deubiquitinases (DUBs) in tissue samples of HNSCC. Notably, aberrant USP14 expression was linked to tumorigenesis and the malignant evolution of HNSCC and further suggested a poor prognosis. In vitro experiment revealed that USP14 depletion markedly inhibited cell growth, cisplatin resistance, invasion and migration capabilities of HNSCC cells. Mechanically, USP14 inhibits FABP5 ubiquitination and degradation, thus positively modulating FABP5 expression. Subsequent analyses demonstrated that the loss of USP14 promoted ferroptosis in HNSCC cells. Finally, in vivo xenograft experiments confirmed that the USP14 small molecular antagonist IU1 could effectively attenuate cisplatin resistance in HNSCC.
conclusionThe results indicate that the USP14-FABP5 axis exerts oncogenic effects on HNSCC, providing a potential target for diagnosing and treating this type of malignancy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.