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NAT10 triggers colorectal cancer progression via promoting PPAN-regulated DNA damage repair

Oncogene volume 45, pages 558–576 (2026)Cite this article

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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.

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Fig. 1: NAT10 is the most significantly upregulated RMRP in CRC and correlated with clinical progression.
Fig. 2: NAT10 facilitates the development of CRC via its ac4C transferase activity.
Fig. 3: NAT10 facilitates the development of CRC by promoting DNA damage repair.
Fig. 4: PPAN mediates the oncogenic roles of NAT10 in CRC.
Fig. 5: NAT10 regulates PPAN expression via modulating its transcription and translation efficiency.
Fig. 6: NAT10 regulates translation of PPAN mRNA via acetylation at the C744 and C747 sites.
Fig. 7: MYBBP1A is an ac4C reader protein for NAT10-regulated PPAN translation.
Fig. 8: MYC mediates NAT10-regulated transcription of PPAN in CRC cells.
Fig. 9: VDR is responsible for the upregulation of NAT10 in CRC cells.
Fig. 10: Oncogenic roles of NAT10-PPAN axis in CRC progression.

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Data availability

The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

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Acknowledgements

We thank Prof Muyan Cai at the Cancer Center of Sun Yat-sen University for plasmid donation, and the staff of Sichuan Higher Education Institute Key Laboratory of Major Disease Target Discovery and Protein Drug Development, and the Irradiation Preservation and Effect Key Laboratory of Sichuan Province.

Funding

This research was supported by the National Natural Science Foundation of China (Nos. 82472761, 82173833, and 82272658), the Guangdong Basic and Applied Basic Research Foundation (Nos. 2023B1515040006, 2021A1515111161, and 2023A1515010118), the Key-Area Research and Development Program of Guangdong Province (No. 2023B1111020007), the Guangzhou Science and Technology Program (No. 2024A04J6480), the Guangdong Provincial Key Laboratory of Construction Foundation (No. 2023B1212060022), the Fundamental Research Funds for the Central Universities (Sun Yat-sen University) (Nos. 24xkjc018, 23qnpy117), the Shenzhen Bay Scholars Program, the Open Fund of Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases (No. 2020B1212060023), the CMC Excellent-talent Program (No. 2024kjTzn03), the Organized Research Projects of Chengdu Medical College (No. CYYZZ24-01), the Clinical Science Research Foundations of Chengdu Medical College (Nos. 2022LHTD-02, 23LHNBZZD07, 24LHBBYY1-08, 24LHBBYY1-09, and 24LHFYSZ1-27).

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  1. These authors contributed equally: Haoran Wang, Lichen Ge, Jianing Li, Ke Zhong.

Authors and Affiliations

  1. Guangdong Provincial Key Laboratory of New Drug Design and Evaluation; State Key Laboratory of Anti-Infective Drug Discovery and Development, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, 510006, China

    Haoran Wang, Jianing Li, Ke Zhong, Shanzhi Li, Ningjing Ma, Lijun Tao, Jiawang Zhou, Zhaotong Wang, Xing Chang, Yunqing Lu, Yalan Rui, Guoyou Xie, Zuanzong Xu, Abdulaziz Ahmed A. Saad, Xiansong Wang, Cheng Yi & Hongsheng Wang

  2. The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital; Chengdu Pidu District People’s Hospital; School of Biological Sciences and Technology, Chengdu Medical College, Chengdu, 610500, China

    Haoran Wang & Kun Zhang

  3. Department of Laboratory Medicine, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China

    Lichen Ge

  4. Department of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China

    Weifeng Yang

  5. Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China

    Zhuojia Chen

  6. The Huadu District People’s Hospital, Guangzhou, China

    Wanglin Li

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  1. Haoran Wang
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Contributions

K Zhang, HS Wang, C Yi, HR Wang, and LC Ge designed and initiated the study. HR Wang, JN Li, K Zhong, SZ Li, NJ Ma, ZZ Xu and YL Rui performed experiments. HR Wang, LC Ge, LJ Tao and JW Zhou, WF Yang wrote the paper. HR Wang, XS Wang and X Chang provided assistance in bioinformatics analysis. WL Li, K Zhang, ZJ Chen, ZT Wang, YQ Lu, Abdulaziz Ahmed A.Saad, and GY Xie in charge of supervision as well as data curation.

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Correspondence to Cheng Yi, Hongsheng Wang or Kun Zhang.

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This study was conducted with approval from the Medical Ethics Committee of Huadu District People’s Hospital, Guangzhou (Approval No. 2025158) and informed consent from all patients, in compliance with the Declaration of Helsinki. Animal experimental protocols were reviewed and approved by the Institutional Animal Care and Use Committee of Sun Yat-sen University (Approval Nos. SYSU-IACUC-2023-001865, SYSU-IACUC-2024-001583).

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Wang, H., Ge, L., Li, J. et al. NAT10 triggers colorectal cancer progression via promoting PPAN-regulated DNA damage repair. Oncogene 45, 558–576 (2026). https://doi.org/10.1038/s41388-025-03661-0

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