98%
921
2 minutes
20
RNA modification has emerged as a crucial area of research in epigenetics, significantly influencing tumor biology by regulating RNA metabolism. N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, the sole known acetylation in eukaryotic RNA, influences cancer pathogenesis and progression. NAT10 is the only writer of ac4C and catalyzes acetyl transfer on targeted RNA, and ac4C helps to improve the stability and translational efficiency of ac4C-modified RNA. NAT10 is highly expressed and associated with poor prognosis in pan-cancers. Based on its molecular mechanism and biological functions, ac4C is a central factor in tumorigenesis, tumor progression, drug resistance, and tumor immune escape. Despite the increasing focus on ac4C, the specific regulatory mechanisms of ac4C in cancer remain elusive. The present review thoroughly analyzes the current knowledge on NAT10-mediated ac4C modification in cancer, highlighting its broad regulatory influence on targeted gene expression and tumor biology. This review also summarizes the limitations and perspectives of current research on NAT10 and ac4C in cancer, to identify new therapeutic targets and advance cancer treatment strategies.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11617596 | PMC |
http://dx.doi.org/10.1002/mco2.70026 | DOI Listing |
Front Genet
August 2025
Hunan Provincial Key Laboratory of Finance and Economics Big Data Science and Technology, Hunan University of Finance and Economics, Changsha, China.
RNA N4-acetylcytidine (ac4C) is a crucial chemical modification involved in various biological processes, influencing RNA properties and functions. Accurate prediction of RNA ac4C sites is essential for understanding the roles of RNA molecules in gene expression and cellular regulation. While existing methods have made progress in ac4C site prediction, they still struggle with limited accuracy and generalization.
View Article and Find Full Text PDFMethods
August 2025
School of Software, Shandong University, Jinan, China. Electronic address:
RNA N4-acetylcytidine (ac4C) modification plays a vital role in gene regulation and cellular function. Accurate identification of ac4C sites is essential for elucidating their biological significance. However, existing prediction methods struggle to capture complex sequence patterns, limiting their accuracy.
View Article and Find Full Text PDFFront Cell Dev Biol
August 2025
Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, Stem Cell and Cancer Center, The First Hospital of Jilin University, Changchun, China.
N4-acetylcytidine (ac4C) is an evolutionarily conserved RNA modification catalyzed by the acetyltransferase NAT10. It regulates RNA stability, translation, and post-transcriptional processes. Meanwhile, NAT10 functions as a dual-function enzyme exhibiting both protein acetyltransferase and RNA acetylase activities.
View Article and Find Full Text PDFInt J Biol Sci
August 2025
Department of General Surgery & Nanfang Gastrointestinal Cancer Institute (NGCI), Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P. R. China.
Tumor vascular normalization has emerged as a promising strategy to potentiate immune checkpoint blockade in solid tumors. Here, we unveil a previously unrecognized NAT10/XIST/YAP1/VEGFA signaling axis driving vascular abnormalization in gastric cancer (GC) and demonstrate its therapeutic potential in remodeling the tumor immune microenvironment. Through integrative analysis of acetylated RNA immunoprecipitation sequencing (acRIP-seq) and functional validation, we identified NAT10-mediated N4-acetylcytidine (ac4C) modification as a critical stabilizer of lncRNA XIST.
View Article and Find Full Text PDFPancreas
September 2025
State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital.
Objectives: To elucidate the role of N-acetyltransferase 10 (NAT10) in pancreatic cancer (PC) progression and its epigenetic mechanisms, particularly in relation to metastasis.
Methods: TCGA and GTEx databases were used to analyze the expression and roles of NAT10 in pancreatic cancer. We constructed stable cell lines with NAT10 knockdown in PC cell lines, AsPC-1 and KPC.