Evidence map›Paper›PMID 38429907›Full record

ArticleJournal of cellular and molecular medicine2024

METTL3 as a novel diagnosis and treatment biomarker and its association with glycolysis, cuproptosis and ceRNA in oesophageal carcinoma.

Xu-Sheng Liu, Yu Zhang, Zi-Yue Liu, Yan Gao, Ling-Ling Yuan, Dao-Bing Zeng, Fan Tan, Hua-Bing Wan, Zhi-Jun Pei

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026
    Review
  5. mFrontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
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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 1 institution in 1 country.

Xu-Sheng LiuDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.ORCID 0000-0002-3663-1096
Yu ZhangDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Zi-Yue LiuDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Yan GaoDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Ling-Ling YuanDepartment of Pathology, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Dao-Bing ZengDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Fan TanDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Hua-Bing WanDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Zhi-Jun PeiDepartment of Nuclear Medicine, Hubei Provincial Clinical Research Center for precision Diagnosis and Treatment of liver cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, China.ORCID 0000-0001-6125-0626
Hubei University of Medicine · CN

Funding

Foundation for Innovative Research Team of Hubei Provincial Department of Education T2020025Hubei province's Outstanding Medical Academic Leader programInnovative Research Program for Graduates of Hubei University of Medicine YC2023007Innovative Research Program for Graduates of Hubei University of Medicine YC2023035Key Discipline Project of Hubei University of MedicineShiyan Taihe Hospital hospital-level project 2022JJXM006Shiyan Taihe Hospital hospital-level project 2022JJXM007the general project of Hubei Provincial Department of Education B2021160
6 · The paper itself

Abstract

METTL3 has been shown to be involved in regulating a variety of biological processes. However, the relationship between METTL3 expression and glycolysis, cuproptosis-related genes and the ceRNA network in oesophageal carcinoma (ESCA) remains unclear. ESCA expression profiles from databases were obtained, and target genes were identified using differential analysis and visualization. Immunohistochemistry (IHC) staining assessed METTL3 expression differences. Functional enrichment analysis using GO, KEGG and GSEA was conducted on the co-expression profile of METTL3. Cell experiments were performed to assess the effect of METTL3 interference on tumour cells. Correlation and differential analyses were carried out to assess the relationship between METTL3 with glycolysis and cuproptosis. qRT-PCR was used to validate the effects of METTL3 interference on glycolysis-related genes. Online tools were utilized to screen and construct ceRNA networks based on the ceRNA theory. METTL3 expression was significantly higher in ESCA compared to the controls. The IHC results were consistent with the above results. Enrichment analysis revealed that METTL3 is involved in multiple pathways associated with tumour development. Significant correlations were observed between METTL3 and glycolysis-related genes and cuproptosis-related gene. Experiments confirmed that interfered with METTL3 significantly inhibited glucose uptake and lactate production in tumour cells, and affected the expression of glycolytic-related genes. Finally, two potential ceRNA networks were successfully predicted and constructed. Our study establishes the association between METTL3 overexpression and ESCA progression. Additionally, we propose potential links between METTL3 and glycolysis, cuproptosis and ceRNA, presenting a novel targeted therapy strategy for ESCA.

Indexed as

CarcinomaEsophageal NeoplasmsMethyltransferasesBiomarkersGlycolysisHumansLactic AcidRNA, Competitive EndogenousBiomarkersLactic AcidMethyltransferasesMETTL3 protein, humanRNA, Competitive EndogenousceRNAcuproptosisglycolysisMETTL3oesophageal carcinoma

Identifiers

PMID38429907
PMCPMC10907846
OpenAlexW4392346127

What OpenQuestion 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 OpenQuestion graph.