ArticleWorld journal of gastrointestinal oncology2024
METTL5 promotes gastric cancer progression
Article in World journal of gastrointestinal oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- METTL5 deficiency impairs osteogenesis through OSER1-dependent antioxidant regulation.JCI insight · 2026Article
- METTL5 regulates SEPHS2-mediated selenoprotein synthesis to promote multiple myeloma survival and progression.Cell death & disease · 2025Article
- METTL5 in physiology and pathology: mechanisms and implications.Frontiers in cell and developmental biology · 2025Review
- Targeting methyltransferase-like 5-mediated sphingomyelin metabolism: A novel therapeutic approach in gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Clinical implications of the latest advances in gastrointestinal tumor research.World journal of gastrointestinal oncology · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe treatment of gastric cancer (GC) has caused an enormous social burden worldwide. Accumulating studies have reported that N6-methyladenosine (m6A) is closely related to tumor progression. METTL5 is a m6A methyltransferase that plays a pivotal role in maintaining the metabolic stability of cells. However, its aberrant regulation in GC has not been fully elucidated.
aimTo excavate the role of METTL5 in the development of GC.
methodsMETTL5 expression and clinicopathological characteristics were analyzed
resultsOur research revealed substantial upregulation of METTL5, which suggested a poor prognosis of GC patients. Increased METTL5 expression indicated distant lymph node metastasis, advanced cancer stage and pathological grade. An increased level of METTL5 correlated with a high degree of m6A methylation. METTL5 markedly promotes the proliferation, migration, and invasion of GC cells
conclusionMETTL5 was found to be an oncogenic driver of GC and may be a new target for therapy since it facilitates GC carcinogenesis through sphingomyelin metabolism and cisplatin resistance.
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