Evidence map›Paper›PMID 35256595›Full record

ArticleCell death & disease2022

Reducing N6AMT1-mediated 6mA DNA modification promotes breast tumor progression via transcriptional repressing cell cycle inhibitors.

Jiongyu Chen, Yixuan Zhuang, Ping Wang, Jinfeng Ning, Wei Liu, Yiteng Huang, Xueqiong Lin, Lin Peng, Donghong Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  10. Serum Folate and Vitamin BDiabetes, metabolic syndrome and obesity : targets and therapy · 2024
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  11. Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Mammalian DNA NMolecular cell · 2023
    Review
  14. Review
  15. Article
  16. RNA Modifications Meet Tumors.Cancer management and research · 2022
    Review
  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

9 authors at 4 institutions in 2 countries.

Jiongyu Chen *Central Laboratory, Cancer Hospital of Shantou University Medical College, 7 Raoping Road, Shantou, Guangdong, 515041, China.
Yixuan Zhuang *Guangdong Provincial Key Laboratory of Breast Cancer Diagnosis and Treatment, Cancer Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, China.
Ping Wang *School of Medical Imaging, Tianjin Medical University, Tianjin, 300203, China.
Jinfeng NingThoracic Department of Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150040, China.
Wei LiuFourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150040, China.
Yiteng HuangHealth Care Center, First Affiliated Hospital of Shantou University Medical College, 52 Southern Dongxia Road, Shantou, Guangdong, 515041, China.
Xueqiong LinDepartment of Clinical Laboratory, Cancer Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, China.
Lin PengCentral Laboratory, Cancer Hospital of Shantou University Medical College, 7 Raoping Road, Shantou, Guangdong, 515041, China. g_lpeng@stu.edu.cn.
Donghong ZhangCenter for Molecular and Translational Medicine, Georgia State University, Research Science Center, 157 Decatur St SE, Atlanta, GA, 30303, USA. dzhang14@gsu.edu.ORCID http://orcid.org/0000-0001-6143-7204
Shantou University · CNHarbin Medical University · CNGeorgia State University · USTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA N6-methyladenosine (6mA) is a novel epigenetic signaling modification in humans and has been implicated in the progression and tumorigenesis of several cancers. However, the function and mechanism of 6mA in breast cancer (BC), the most common cancer among women, are unclear. Here, we found that decreases in N6AMT1 correlated with the extent of 6mA in clinical BC tissues and predicted a worse survival of BC patients. Functionally, knockdown of N6AMT1 markedly reduced 6mA in DNA and promoted colony formation and migration of BC cells, whereas overexpression of N6AMT1 had the opposite effect. Moreover, silencing of N6AMT1 reduced 6mA modification and enhanced the growth of BC cells in vitro and tumors in vivo. 6mA immunoprecipitation sequencing (6mA-IP-seq), RNA-seq, 6mA-IP-PCR, and bioinformatics analysis indicated that N6AMT1 was a functional methyltransferase for genomic 6mA DNA modifications and related to gene transcriptional activity. Critical negative regulators of the cell cycle, such as RB1, P21, REST, and TP53 were identified as targets of N6AMT1 in BC. These results suggest N6AMT1 enhances DNA 6mA levels to repress tumor progression via transcriptional regulation of cell cycle inhibitors.

Indexed as

Breast NeoplasmsGenomeCell CycleDNADNA MethylationFemaleHumansSite-Specific DNA-Methyltransferase (Adenine-Specific)DNAN6AMT1 protein, humanSite-Specific DNA-Methyltransferase (Adenine-Specific)

Identifiers

PMID35256595
PMCPMC8901905
OpenAlexW4220924661

What OpenQuestion holds

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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.