Evidence map›Paper›PMID 28859621›Full record

ArticleBMC cancer2017

NAT10 is upregulated in hepatocellular carcinoma and enhances mutant p53 activity.

Qijiong Li, Xiaofeng Liu, Kemin Jin, Min Lu, Chunfeng Zhang, Xiaojuan Du, Baocai Xing

Abstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

  1. Article
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  7. The NAT10/acCell communication and signaling : CCS · 2026
    Review
  8. Review
  9. Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. NAT10 andScience advances · 2025
    Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

6 more citing papers are in PubMed but not listed here.

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

7 authors.

Qijiong LiDepartment of Hepatobiliary Oncology, Sun Yat-Sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, Guangdong, 510060, China.
Xiaofeng LiuDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Kemin JinHepatopancreatobiliary Surgery Department I, Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University School of Oncology, Beijing Cancer Hospital and Institute, 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Min LuDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Chunfeng ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Xiaojuan DuDepartment of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Baocai XingHepatopancreatobiliary Surgery Department I, Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University School of Oncology, Beijing Cancer Hospital and Institute, 52 Fucheng Road, Haidian District, Beijing, 100142, China. xingbaocai88@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundN-acetyltransferase 10 (NAT10) is a histone acetyltransferase which is involved in a wide range of cellular processes. Recent evidences indicate that NAT10 is involved in the development of human cancers. Previous study showed that NAT10 acetylates the tumor suppressor p53 and regulates p53 activation. As Tp53 gene is frequently mutated in hepatocellular carcinoma (HCC) and associates with the occurrence and development of HCC, the relationship between NAT10 and HCC was investigated in this study.

methodsImmunohistochemistry (IHC) and western blot analysis were performed to evaluate the NAT10 expression in HCC. Immunoprecipitation experiments were performed to verify the interaction of NAT10 with mutant p53 and Mdm2. RNA interference and Western blot were applied to determine the effect of NAT10 on mutant p53. Cell growth curve was used to examine the effect of NAT10 on HCC cell proliferation.

resultsNAT10 was upregulated in HCC and increased NAT10 expression was correlated with poor overall survival of the patients. NAT10 protein levels were significantly correlated with p53 levels in human HCC tissues. Furthermore, NAT10 increased mutant p53 levels by counteracting Mdm2 action in HCC cells and promoted proliferation in cells carrying p53 mutation.

conclusionIncreased NAT10 expression levels are associated with shortened patient survival and correlated with mutant p53 levels. NAT10 upregulates mutant p53 level and might enhance its tumorigenic activity. Hence, we propose that NAT10 is a potential prognostic and therapeutic candidate for p53-mutated HCC.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, HepatocellularHumansLiver NeoplasmsMiddle AgedMutationN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesPrognosisProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Up-RegulationMDM2 protein, humanNAT10 protein, humanN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Hepatocellular carcinomaMutant p53NAT10PrognosisStability

Identifiers

PMID28859621
PMCPMC5579925

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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.