ArticleOncogene2026
NAT10 triggers colorectal cancer progression via promoting PPAN-regulated DNA damage repair.
Article in Oncogene, 2026. 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
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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.
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
- The RNA helicase domain of NAT10 promotes the biogenesis of hypomodified ribosomes to enhance cancer cell proliferation.Nature communications · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
- FBXO6 mediated ubiquitination of SLC3A2 drives ferroptosis in ulcerative colitis: a machine learning and SHAP discovery.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- ESPNP promotes cell migration and invasion in gastric cancer cells via regulation of epithelial-mesenchymal transition/Twist1.Journal of molecular histology · 2026Article
- Synergistic Effect of Fecal Microbiota Transplantation, γδT Cell Immunotherapy, and Pembrolizumab in Refractory Advanced Pancreatic Cancer: A Case Report.Journal of gastrointestinal cancer · 2026Article
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 2026Review
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
RNA modification recognition proteins are crucial in cancer development and progression. Among all RNA modification-related proteins (RMRPs), Weighted Gene Co-expression Network Analysis (WGCNA), combined with comprehensive bioinformatic analysis, suggests that NAT10-the sole known writer of N4-acetylcytidine (ac4C)-is a critical regulatory protein in colorectal cancer (CRC) progression. NAT10 facilitates the malignancy phenotypes and DNA damage repair in CRC cells via its ac4C transferase activity and regulation of PPAN. Specifically, NAT10 enhances the translation efficiency of PPAN via acetylation at the C744 and C747 sites. In addition, NAT10 promotes the translation of ac4C-modified MYC mRNA. MYC protein then enhances PPAN transcription through binding to the PPAN promoter. The newly identified ac4C reader protein MYBBP1A mediates NAT10-induced translation of both PPAN and MYC. We further found that VDR binds to the NAT10 promoter to activate its transcription, resulting in the high expression of NAT10 in CRC. Xenograft studies and clinical data confirmed the role of the NAT10-PPAN axis in promoting CRC development and DNA damage repair. Collectively, our study reveals the role and underlying mechanism of mRNA ac4C modification in CRC progression, providing critical potential targets for CRC drug development.
Indexed as
Identifiers
41455833What 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.