ArticleBMC women's health2025
NAT10 promotes ovarian cancer cell migration, invasion, and stemness via N4-acetylcytidine modification of CAPRIN1.
Article in BMC women's health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- Review
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- RNA modifications in cancer stem cells: molecular mechanisms and targeted therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer (OC) is the most lethal gynecological tumor. N4-acetylcytidine (ac4C) modification, catalyzed by the acetyltransferase NAT10, is involved in the occurrence and development of cancers. This study aimed to investigate the role of NAT10 in OC and the underlying molecular mechanisms. The expression of NAT10 and CAPRIN1 in OC cells lines were measured using quantitative real-time polymerase chain reaction and immunoblotting. Biological behaviors of OC cells were evaluated using EdU, Transwell, sphere formation, and immunoblotting assays. The molecular mechanism of NAT10 function was analyzed using bioinformatics, ac4C- RNA immunoprecipitation, and actinomycin D treatment assay. The effect of NAT10 on OC progression in vivo was evaluated using xenograft tumor model. The results indicated that NAT10 and CAPRIN1 were highly expressed in OC cells. NAT10 knockdown suppressed OC cell proliferation, migration, invasiveness, stemness, and epithelial-mesenchymal transition in vitro, and impeded tumor growth in vivo. Additionally, CAPRIN1 expression was found to be positively related to NAT10 expression in OC. Silencing of NAT10 inhibited ac4C levels of CAPRIN1 and reduced its RNA stability. Moreover, overexpression of CAPRIN1 reversed the suppression of migration, invasion, and stemness caused by NAT10 knockdown, while knockdown of CAPRIN1 alone inhibited these malignant behaviors of OC cells. In conclusion, NAT10 promotes OC progression by promoting cellular migration, invasion, and stemness via upregulating CAPRIN1 expression. Mechanistically, NAT10 stabilizes CAPRIN1 by promoting its ac4C modification. These findings suggest that NAT10 may be a promising therapy target for OC.
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.