ArticleFrontiers in oncology2025
The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Targeting the METTL5-MGST1 axis for cancer therapy: molecular mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- Inhibition of YTHDF2-mediated CYLD mRNA degradation promotes neuronal ferroptosis and pain in Parkinson's disease through NOX4 deubiquitination.Cell biology and toxicology · 2026Article
- Inhibition ofACS omega · 2025Article
- Inhibition ofbioRxiv : the preprint server for biology · 2025Article
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2 authors.
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Abstract
Background: N6-Methyladenosine (m6A) is one of the post-transcriptional modifications and abnormal m6A is critical for cancer initiation, progression, metastasis in Lung squamous cell carcinoma (LUSC). Ribosomal RNA (rRNA) accounts for most of the total cellular RNA, however, the functions and molecular mechanisms underlying rRNA modifications in LUSC remained largely unclear. Methods: High-throughput library screening identifies the key m6A regulator METTL5 in LUSC. Cell and animal experiments were used to identify that METTL5 promoted LUSC tumorigenesis to enhance DEP domain containing 1 (DEPDC1) translation via m6A modification. Results: We showed that the N6-methyladenosine (m6A) methyltransferase METTL5 was an independent risk factor in LUSC and was associated with poor prognosis of patients. Notedly, overexpression METTL5 promoted LUSC tumorigenesis in an m6A modification, while METTL5 knockdown markedly inhibited proliferation and migratory ability of tumor cells Conclusion: Our results revealed that METTL5 enhances DEPDC1 translation to contribute to tumorigenesis and poor prognosis, providing a potential prognostic biomarker and therapeutic target for LUSC.
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