Evidence map›Paper›PMID 37863889›Full record

ArticleNature communications2023

Lactylation of METTL16 promotes cuproptosis via m

Lianhui Sun, Yuan Zhang, Boyu Yang, Sijun Sun, Pengshan Zhang, Zai Luo, Tingting Feng, Zelin Cui, Ting Zhu, Yuming Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 345 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
345citing papers in PubMed, 2 pooled it
57.6field-weighted citation impact, top 1% 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

345 citing papers in PubMed, 2 syntheses or guidelines pooled it, 372 citations in OpenAlex.

  1. Pooled it
  2. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Lactylation Modification and Esophageal Cancer: Research Progress From Hypoxia-Induced Metabolic Reprogramming to Immune Escape.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  16. Article
  17. WTAP Transcriptional Suppression by KLF9 Drives Osteoclastogenesis via MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  18. Article
  19. Article
  20. Review

285 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

13 authors at 2 institutions in 1 country.

Lianhui Sun *Department of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yuan Zhang *Department of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.ORCID 0000-0001-9284-9404
Boyu Yang *Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Sijun Sun *Department of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Pengshan ZhangDepartment of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Zai LuoDepartment of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Tingting FengDepartment of Clinical Pharmacy, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Zelin CuiDepartment of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.ORCID 0000-0002-2700-5800
Ting ZhuPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yuming LiDepartment of Critical Care Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Zhengjun QiuDepartment of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Guangjian FanPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. gjfan@shsmu.edu.cn.ORCID 0000-0003-0684-1380
Chen HuangDepartment of Gastrointestinal Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. richard-hc@hotmail.com.ORCID 0000-0003-0404-461X
Shanghai Jiao Tong University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cuproptosis, caused by excessively high copper concentrations, is urgently exploited as a potential cancer therapeutic. However, the mechanisms underlying the initiation, propagation, and ultimate execution of cuproptosis in tumors remain unknown. Here, we show that copper content is significantly elevated in gastric cancer (GC), especially in malignant tumors. Screening reveals that METTL16, an atypical methyltransferase, is a critical mediator of cuproptosis through the m

Indexed as

ApoptosisStomach NeoplasmsCopperHumansHydrazinesLactic AcidMethyltransferasesRNA, MessengerSirtuin 2CopperelesclomolHydrazinesLactic AcidMethyltransferasesMETTL16 protein, humanRNA, MessengerSirtuin 2

Identifiers

PMID37863889
PMCPMC10589265
OpenAlexW4387815001

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.