ArticleMolecular and cellular biochemistry2025
METTL16 promotes progression of clear cell renal cell carcinoma via up-regulating N6-methyladenosine modification of KLK4 mRNA.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Beyond mBiomedicines · 2026Review
- CDK13 drives clear cell renal carcinoma through METTL16-mediated mExperimental & molecular medicine · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
The advancement of clear cell renal cell carcinoma (ccRCC) is a significant problem in clinical practice, and understanding the molecular determinants of malignancy progression is essential for the creation of viable treatment targets. METTL16, a methyltransferase enzyme responsible for RNA modifications, has been linked to a variety of cancers. However, its specific role in ccRCC remain unclear. The function of METTL16 was validated using in vivo and in vitro gain/loss of function experiments. Our functional assays indicated that silencing METTL16 significantly impaired cell proliferation, migration, and invasive capabilities. Mechanistically, MeRIP-PCR and luciferase assays confirmed that METTL16 promoted m6A modification of KLK4 and enhanced its stability through recognition of the m6A reader protein, IGF2BP2. KLK4 overexpression reversed the proliferation and migration defects caused by METTL16 knockdown, possibly through activation of ERK and AKT signaling pathways. In vivo experiments further demonstrated that KLK4 overexpression mitigated tumor growth inhibition caused by METTL16 depletion. These findings suggest that METTL16 promotes ccRCC progression via KLK4-mediated signaling, highlighting a potential therapeutic target.
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Registered trials
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