ArticleTranslational cancer research2026
Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Background: N4-acetylcytidine (ac4C) is an RNA epigenetic modification, newly discovered to be catalyzed by the enzyme N-acetyltransferase 10 (NAT10). This study aimed to elucidate the functional role and regulatory mechanism of NAT10-mediated ac4C RNA modification in head and neck squamous cell carcinoma (HNSCC), and to explore its potential as a druggable target. Methods: Bioinformatics analysis of The Cancer Genome Atlas (TCGA) data was performed to assess NAT10 expression and its clinical correlation in HNSCC. Gene set enrichment analysis (GSEA) was conducted on differentially expressed genes from NAT10-high versus NAT10-low patients. The L1000 FireWorks Display (L1000FWD) platform was utilized to predict potential NAT10-targeting drugs. The anti-tumor effects and mechanisms of the top candidate, quetiapine, were validated through Results: NAT10 was significantly upregulated in HNSCC, and its high expression was correlated with advanced tumor stage, higher grade, poor overall survival, and specific immune cell infiltration patterns. GSEA revealed a strong association between NAT10 and the oxidative phosphorylation (OXPHOS) pathway. Quetiapine was identified as a top candidate targeting the NAT10-associated signature. Conclusions: NAT10 functions as a critical oncoprotein in HNSCC, potentially by enhancing OXPHOS-driven energy metabolism. The repurposed drug quetiapine suppresses tumor growth by targeting the NAT10/ac4C axis and disrupting mitochondrial respiratory function, positioning it as a promising therapeutic agent for HNSCC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.