Evidence map›Paper›PMID 32428852›Full record

ArticleTranslational oncology2020

N-Acetyltransferase 10 Promotes Micronuclei Formation to Activate the Senescence-Associated Secretory Phenotype Machinery in Colorectal Cancer Cells.

Yanan Cao, Mengfei Yao, Yaqian Wu, Ningning Ma, Haijing Liu, Bo Zhang

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.8field-weighted citation impact, top 4% of its field
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

40 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Oncogenic role of LncRNA DLEU2 in thyroid cancer through a NAT10/USP39 regulatory axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  4. Article
  5. The NAT10/acCell communication and signaling : CCS · 2026
    Review
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  7. Article
  8. Article
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  10. Article
  11. Review
  12. Article
  13. Review
  14. The N-acetyltransferase 10 inhibitor [EJNMMI radiopharmacy and chemistry · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Review
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  20. Article
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 at 1 institution in 1 country.

Yanan CaoDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Mengfei YaoDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Yaqian WuDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Ningning MaDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Haijing LiuDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Bo ZhangDepartment of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100191, China. Electronic address: zhangbo@bjmu.edu.cn.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The formation of micronuclei (MN) is prevalent in human cancer cells and its role in activating the senescence-associated secretory phenotype (SASP) machinery has been identified recently. However, the role of MN in regulation of SASP signaling still needs to define in practical cancers. Here, we reported that in colorectal cancer cells the expression of NAT10 (N-acetyltransferase 10) could mediate MN formation through DNA replication and NAT10-positive MN could activate SASP by binding to cGAS. The chemical inhibition of NAT10 by Remodelin or genomic depletion could markedly reduce MN formation, SASP activation, and senescence in colorectal cancer cells. Cell stress such as oxidative or hypoxia could upregulate NAT10 and its associated MN formation senescence and expression of SASP factors. Statistical analysis of clinical specimens revealed correlations between NAT10 expression, MN formation, SASP signaling, and the clinicopathological features of colorectal cancer. Our data suggest that NAT10 increasing MN formation and SASP pathway activation, promoting colorectal cancer progression.

Identifiers

PMID32428852
PMCPMC7232111
OpenAlexW3025438382

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.