ArticleCell death & disease2025
USP10 stabilizes BAZ1A to drive tumor stemness via an epigenetic mechanism in head and neck squamous cell carcinoma.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- Article
- Review
- NAA20-mediated ACF1 lactylation drives neuroblastoma progression through enhancing GCLM-dependent glutathione synthesis.Cell biology and toxicology · 2026Article
- Ubiquitin-Specific Protease 10: A New Target in Tumor Immune Escape.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant epigenetic remodeling events occurred in head and neck squamous cell carcinoma (HNSCC) contribute to tumor stemness and chemotherapy resistance, yet little is known. In this study, we identified that ubiquitin-specific peptidase 10 (USP10) is up-regulated in HNSCC tissues, and high USP10 is associated with poor prognosis of patients. Functionally, USP10 serving as an oncogene potentiates the proliferation and metastasis of HNSCC cells in vitro and in vivo. Mechanistically, USP10 physically interacts with, deubiquitinate, and stabilizes BAZ1A proteins. In addition, BAZ1A complexes with SOX2 to drive the enhancer-promoter interaction and facilitate the recruitment of BRD4, thereby activating the expressions of cancer stem cells (CSCs)-related signature. Therefore, we found that USP10 relied on BAZ1A to enhance HNSCC stemness, progression, and chemotherapy resistance. The pharmacology research implicated that BAZ1A-IN-1, one specific BAZ1A inhibitor, could effectively inhibit HNSCC stemness, distal metastasis, and cisplatin resistance. Together, our study revealed a novel USP10/BAZ1A/stemness axis and one significant therapeutic target for USP10-driven HNSCC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.