Evidence map›Paper›PMID 39648231›Full record

ArticleMolecular biomedicine2024

Acetyltransferase NAT10 promotes an immunosuppressive microenvironment by modulating CD8

Ji Liu, Zhuoran Gu, Libin Zou, Zhijin Zhang, Liliang Shen, Ruiliang Wang, Shaobo Xue, Jiang Geng, Shiyu Mao, Wentao Zhang and 1 more

Abstract read
In one paragraph

Article in Molecular biomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Review
  2. Review
  3. NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. The NAT10/acCell communication and signaling : CCS · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

11 authors.

Ji Liu *Department of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Zhuoran Gu *Department of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Libin Zou *Department of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Zhijin ZhangDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Liliang ShenDepartment of Urology, the Affiliated People's Hospital of Ningbo University, 251 East Baizhang Road, Ningbo City, Zhejiang Province, 315040, China.
Ruiliang WangDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Shaobo XueDepartment of Central Laboratory, Clinical Medicine Scientific and Technical Innovation Park, Shanghai Tenth People's Hospital, Shanghai, 200435, China.
Jiang GengDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Shiyu MaoDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. maoshiyu1144@sina.com.
Wentao ZhangDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. zhangwentao98@163.com.
Xudong YaoDepartment of Urology, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. yaoxudong1967@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-acetyltransferase 10 (NAT10), an enzyme responsible for ac4C acetylation, is implicated in cancer progression, though its specific biological function in prostate cancer remains insufficiently understood. This study clarifies NAT10's role in prostate cancer and its effects on the tumor immune microenvironment. NAT10 expression and clinical relevance were assessed through bioinformatics, RT-qPCR, and IHC analyses, comparing prostate cancer tissues with normal controls. The impact of NAT10 on tumor cell proliferation, migration, and invasion was investigated via in vitro assays-including CCK-8, EdU, wound healing, and 3D-Transwell-as well as in vivo mouse xenograft models and organoid studies. Further, NAT10's influence on immune cell infiltration was examined using flow cytometry, IHC, cell co-culture assays, and ELISA to elucidate downstream chemokine effects, specifically targeting CD8

Indexed as

CD8-Positive T-LymphocytesCell ProliferationProstatic NeoplasmsTumor MicroenvironmentAnimalsCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansMaleMiceN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesReceptors, CCRCC chemokine receptor 9NAT10 protein, humanN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesReceptors, CCRAc4C acetylationImmune microenvironmentImmunotherapyProstate cancer

Identifiers

PMID39648231
PMCPMC11625704

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Registered trials

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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.