Evidence map›Paper›PMID 41112236›Full record

ReviewFrontiers in immunology2025

The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity.

Chunhong Li, Xiulin Jiang, YingDong Jia, Qiang Zhou, Yixiao Yuan, Qiang Wang

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Machine learning identifies ac4C-related prognostic signature and TUBA1C as therapeutic target in COAD.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Chunhong LiDepartment of Oncology, Suining Central Hospital, Suining, Sichuan, China.
Xiulin JiangDepartment of Systems Biology, City of Hope Comprehensive Cancer Center Biomedical Research Center, Monrovia, CA, United States.
YingDong JiaDepartment of Gastrointestinal Surgical Unit, Suining Central Hospital, Suining, Sichuan, China.
Qiang ZhouDepartment of Oncology, Suining Central Hospital, Suining, Sichuan, China.
Yixiao YuanDepartment of Systems Biology, City of Hope Comprehensive Cancer Center Biomedical Research Center, Monrovia, CA, United States.
Qiang WangDepartment of Gastrointestinal Surgical Unit, Suining Central Hospital, Suining, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NAT10, a conserved RNA acetyltransferase, installs N4-acetylcytidine (ac4C) on RNA, thereby regulating stability and translation. Beyond tumor cell proliferation, DNA repair, and chromatin remodeling, NAT10 shapes the tumor immune microenvironment, influencing immune evasion, immune cell infiltration, and responses to immunotherapy. Preclinical studies highlight NAT10 inhibition, such as with Remodelin, as a strategy to enhance cancer treatment-alone or combined with checkpoint blockade, adoptive cell transfer, or chemoradiotherapy. Remaining challenges include

Indexed as

CytidineNeoplasmsAnimalsHumansTumor MicroenvironmentCytidineN-acetylcytidinecancer immunotherapyimmune checkpointsimmune regulationN4-acetylcytidine (ac4C)NAT10RNA acetylationtumor immunity

Identifiers

PMID41112236
PMCPMC12528087

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.