ArticleCell division2025
METTL16 accelerates lung adenocarcinoma progression by inducing N6-methyladenosine modification of GTSE1 to regulate p53 pathway and cell cycle.
Article in Cell division, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Development and Validation of an m6A-Derived Prognostic Signature in Lung Adenocarcinoma.Journal of Cancer · 2026Article
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2 authors.
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Abstract
backgroundMETTL16 has recently emerged as an N6-methyladenosine (m
methodsThe expression of METTL16 and G2 and S phase-expressed-1 (GTSE1) in LUAD was evaluated by qRT-PCR or western blotting. LUAD cell malignancy was checked by CCK-8, wound healing, and transwell invasion assays. The relationship among METTL16 and GTSE1 was determined via Pearson correlation analysis and MeRIP assay. The p53 pathway-related proteins were detected by western blotting, and cell cycle was analyzed by flow cytometry.
resultsMETTL16 was elevated in LUAD, and its silencing significantly reduced LUAD cell proliferation, migration, and invasion. GTSE1 was significantly downregulated upon silencing METTL16. Furthermore, increased levels of GTSE1 mRNA and protein were found in LUAD, and it was correlated positively with METTL16 in LUAD tissues. The stability of GTSE1 was modulated by METTL16 in an m
conclusionsThese results indicate that METTL16-mediated m
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