ArticleCancer medicine2025
USP5 Promotes Head and Neck Squamous Cell Carcinoma Progression via mTOR Signaling Pathway.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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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
2 citing papers in PubMed.
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- USP5 promotes glycolysis in cervical cancer by stabilizing FOXM1.American journal of cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHead and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy characterized by limited prognostic markers and treatment options, contributing to high mortality rates. While Ubiquitin-specific peptidase 5 (USP5) has been implicated in various cancers, its role in HNSCC remains poorly understood.
aimsThis study aims to investigate the role of USP5 in the progression of HNSCC and explore its potential as both a prognostic biomarker and a therapeutic target. MATERIALS &
methodsThis work utilized single-cell transcriptomic analysis with the Scissor algorithm to identify distinct epithelial subpopulations, particularly focusing on the Stress subpopulation that exhibited significant upregulation of USP5. Validation was conducted using tissue microarray (TMA) analysis and immunohistochemistry (IHC) to compare USP5 expression levels in HNSCC tissues versus adjacent normal tissues. Furthermore, RNA interference (RNAi) experiments were performed to knock down USP5 expression, assessing its effects on tumor cell behavior, including proliferation, migration, and invasion, as well as the regulation of mTORC1 and NF-κB signaling pathways.
resultsThis study revealed that the Stress subpopulation, characterized by USP5 upregulation, was associated with enhanced tumor cell proliferation, migration, and invasion. TMA and IHC analyses confirmed that USP5 expression was significantly higher in HNSCC tissues compared to normal tissues, correlating with poor patient prognosis. Additionally, RNAi-mediated knockdown of USP5 led to reduced tumor cell activities and downregulation of the mTORC1 and NF-κB signaling pathways. DISCUSSION: The findings suggest that USP5 plays a critical role in driving HNSCC progression. Its overexpression in aggressive tumor subpopulations and association with poor clinical outcomes highlight its potential utility as both a prognostic biomarker and a therapeutic target. The observed effects on cell behavior and oncogenic signaling pathways provide mechanistic insights into how USP5 for HNSCC therapy.
conclusionsThis study establishes USP5 as a key driver of HNSCC progression, underscoring its potential role in prognosis and therapy. Targeting USP5 may offer novel treatment strategies for HNSCC, addressing the urgent need for effective therapeutic interventions in this aggressive 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.