Evidence map›Paper›PMID 41114928›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

METTL10-Mediated PIAS3 Methylation Links Purine Metabolism to Gastric Cancer Progression.

Jinshui Tan, Huiwen Zhou, Jingsong Ma, Chensong Zhang, Yuhua Tan, Baoding Zhang, Jiabao Zhao, Ao Cheng, Chengyu Yang, Meijuan Xu and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. METTL10-Mediated PIAS3 Methylation Links Purine Metabolism to Gastric Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

21 authors.

Jinshui TanDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Huiwen ZhouDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Jingsong MaDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Chensong ZhangState Key Laboratory for Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, 361104, China.
Yuhua TanState Key Laboratory for Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, 361104, China.
Baoding ZhangState Key Laboratory for Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, 361104, China.
Jiabao ZhaoDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Ao ChengDepartment of Surgical Oncology and General Surgery, Key Laboratory of Precision Diagnosis and Treatment of Gastrointestinal Tumors, Ministry of Education, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Chengyu YangState Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Public Health, Xiamen University, Xiamen, Fujian, 361102, China.
Meijuan XuDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Shengyi ZhouDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Yubo XiongDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Zeyang LinDepartment of Pathology, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Guangchao PanDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Wenjie YeDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Mengya ZhongDepartment of Radiology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, 361003, China.
Yang YangDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Yifan ZhuangDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.
Shao-Wei LiState Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Public Health, Xiamen University, Xiamen, Fujian, 361102, China.
Xianming DengDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.ORCID https://orcid.org/0000-0002-9354-5864
Xuehui HongDepartment of Gastrointestinal Surgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361004, China.ORCID https://orcid.org/0000-0002-8853-7384

Funding

the Fujian Health Youth Scientific Research Project 2021ZQNZD018the National Natural Science Foundation of China 82072727the National Natural Science Foundation of China 82103160the National Natural Science Foundation of China 82122046the Young Top Talents of Fujian Young Eagle Project
6 · The paper itself

Abstract

Metabolic dysregulation plays a significant role in the development of gastric cancer (GC). However, the mechanisms that control this change and its impact on GC progression remain poorly understood. In this study, it is demonstrated that methyltransferase-like 10 (METTL10) is a key regulator of gastric tumor formation by enhancing purine metabolism in GC cells. It is discovered that METTL10 methylates the protein inhibitor of activated STAT3 (PIAS3) at the lysine 442 (K442) residue, which interferes with the interaction of PIAS3 with microphthalmia-associated transcription factor (MITF). As a result, the sumoylation and ubiquitination of MITF by PIAS3 are reduced, leading to MITF stabilization and activation of purine metabolism. Importantly, both the accumulation of MITF and the methylation of K442 in PIAS3 are required for the oncogenic effects of METTL10, and both factors are closely linked to poor clinical outcomes in GC. Furthermore, this study identified a compound, LZQ-02-023-01, which effectively induces the METTL10-mediated ubiquitination and degradation of MITF, thereby reducing the oncogenic activity of METTL10. The findings suggest that METTL10 plays an important role in reprogramming purine metabolism, which promotes GC, highlighting it as a potential therapeutic target for GC treatment.

Indexed as

MethyltransferasesMolecular ChaperonesProtein Inhibitors of Activated STATPurinesStomach NeoplasmsAnimalsCell Line, TumorDisease ProgressionHumansMethylationMiceMethyltransferasesMolecular ChaperonesPIAS3 protein, humanProtein Inhibitors of Activated STATpurinePurinesMethylationMETTL10MITFPIAS3Purine metabolism

Identifiers

PMID41114928
PMCPMC12752606

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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.