ArticleEuropean journal of medical research2025
Mechanism of methyltransferase METTL14 mediating m6A modification and regulating SIRT5 expression to promote ferroptosis and repress gastric cancer progression.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Emerging Role of Sirtuins-Mediated Ferroptosis in Hepatocellular Carcinoma Progression: Mechanisms and Therapeutic Perspectives.Journal of hepatocellular carcinoma · 2026Review
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesGastric cancer (GC) ranks as the third leading reason of cancer-associated deaths worldwide. This study investigates the mechanism by which the m6A methyltransferase methyltransferase-like 14 (METTL14) enhances ferroptosis and inhibits GC progression through regulation of sirtuin 5 (SIRT5).
methodsIn vitro, AGS cells were treated with pcDNA3.1-METTL14, si-SIRT5 and Ferrostatin-1, while NCI-N87 cells were transfected with si-METTL14. Expression levels of METTL4 and SIRT5 were measured using RT-qPCR and Western blot. GC cell proliferation, migration, and invasion were evaluated through CCK-8, colony formation, and transwell assays. The SRAMP database was used to predict m6A modification sites on SIRT5 mRNA. Interaction between METTL14 and SIRT5 was assessed by RIP assay, with subsequent analysis of SIRT5 m6A modification and SIRT5 mRNA stability via Me-RIP assay and actinomycin D treatment. Reactive oxygen species, Fe
resultsMETTL14 expression was significantly reduced in GC cell lines. METTL14 overexpression suppressed GC cell proliferation, invasion, and migration. Mechanistically, METTL14 increased SIRT5 mRNA stability through m6A modification. Silencing of SIRT5 partially counteracted the inhibitory effects of METTL14 overexpression on GC cell malignancy. METTL14 promoted ferroptosis and inhibited GC cell malignancy through SIRT5. In vivo, METTL14 overexpression reduced GC tumor growth by upregulating SIRT5 expression.
conclusionsMETTL14 stabilizes SIRT5 mRNA via m6A modification, upregulating SIRT5 expression and inducing ferroptosis, thereby inhibiting GC progression.
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