ArticleCancer science2025
METTL14 attenuates cancer stemness by suppressing ATF5/WDR74/β-catenin axis in gastric cancer.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Potential Role of METTL14 in Modulating Prostate Cancer Proliferation and Glycolysis Through m6A Modification of LINC01138.Applied biochemistry and biotechnology · 2026Article
- Gene Variations in RNA Modification Pathway Linked to Poor Survival After Gastric Cancer Surgery.Genes · 2026Article
- The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.Oncogene · 2026Review
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- Role of histone modifications in gastric cancer (Review).International journal of oncology · 2026Review
- The potential of ATF5 as a prognostic marker and therapeutic target in cancer: insights from bioinformatics analysis and experimental validation.Translational cancer research · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Chlorogenic acid promotes mtDNA leakage to enhance cGAS-STING induced anti-tumor immunity via ATF5-mtHSP70-TFAM system.International journal of biological sciences · 2026Article
- RNA modifications in cancer stem cells: molecular mechanisms and targeted therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- Targeting Lactylation for Cancer: Mechanisms, Effects, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Review
- Lactylation in cancer biology: Unlocking new avenues for research and therapy.Cancer communications (London, England) · 2025Review
- Lactate and lactylation: molecular insights into histone and non-histone lactylation in tumor progression, tumor immune microenvironment, and therapeutic strategies.Biomarker research · 2025Review
- The mMolecular biomedicine · 2025Review
- Crosstalk between lactylation and RNA modifications in tumorigenesis: mechanisms and therapeutic implications.Biomarker research · 2025Review
- hnRNPU-mediated pathogenic alternative splicing drives gastric cancer progression.Journal of experimental & clinical cancer research : CR · 2025Article
- The inspiration of methyltransferase in RNA methylation modification for targeted therapy of malignant tumors.Frontiers in immunology · 2025Review
- Activating Transcription Factor 5 Promotes Tumorigenic Capability in Cervical Cancer Through the Wnt/β-Catenin Signaling Pathway.Cancer management and research · 2025Article
- METTL14 attenuates cancer stemness by suppressing ATF5/WDR74/β-catenin axis in gastric cancer.Cancer science · 2025Article
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7 authors.
Funding
Abstract
Stemness is a key factor contributing to treatment failure in gastric cancer (GC). Methyltransferase-like 14 (METTL14) has been linked to various cancers, though its specific role in regulating stemness in GC remains undefined. In this study, we assessed METTL14 expression levels in GC tissues using public datasets and clinical specimens and investigated its impact on cell proliferation, metastasis, and stemness both in vitro and in vivo. Through m6A RNA immunoprecipitation (MeRIP) and luciferase reporter assays, we identified downstream targets of METTL14. Rescue assays were performed to examine whether METTL14 overexpression could reverse stemness in GC. We also explored the underlying mechanisms using chromatin immunoprecipitation (ChIP) and western blot analysis, focusing on the role of ATF5 and the upstream regulation of METTL14. Our findings show that lower METTL14 expression is associated with poorer overall survival in GC patients. Functionally, METTL14 knockdown enhanced stemness traits in GC cells. Mechanistically, METTL14 facilitated m6A modification, promoting the degradation of ATF5 mRNA. Overexpression of ATF5 reversed the stemness inhibition caused by METTL14 overexpression by increasing WDR74 transcription and enhancing β-catenin nuclear translocation. Furthermore, histone H3 lactylation at Lys18 was found to upregulate METTL14 expression. In conclusion, METTL14 knockdown promotes stemness in GC by mediating m6A modification of ATF5 mRNA, which activates the WDR74/β-catenin axis, making METTL14 a potential therapeutic target for gastric cancer treatment.
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