ArticleMedical oncology (Northwood, London, England)2026
METTL14-mediated FDX1 m6A methylation inhibited the proliferation of clear cell renal cell carcinoma.
Article in Medical oncology (Northwood, London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
FDX1 exerts a significant influence in the process of cuproptosis by facilitating the lipoacylation of proteins and reducing copper ions to monovalent copper ions. The methyltransferase METTL14 is an enzyme that modulates the m6A methylation of RNA, which can impact the stability, translation efficiency, and degradation rate of RNA. Nevertheless, the regulatory association between METTL14 and FDX1 in kidney cancer requires further investigation. The differential expression of METTL14 and FDX1 between normal tissues and renal cancer tissues was analyzed via the GEO public database. The association between these factors and patient survival was analyzed by utilizing the TCGA public database. A correlation analysis between METTL14 and FDX1 was performed based on the TCGA database. The findings were validated through RT - qPCR, Western blot, and immunohistochemistry assays. By using SRAMP tools and m6A correlation experiments, the study elucidated the reason for the decreased expression of FDX1 in renal cancer cells. In vivo and in vitro experiments were conducted to verify the regulatory effect of METTL14 on FDX1. In clear cell renal cell carcinoma (ccRCC), METTL14 and FDX1 exhibit downregulation and are correlated with a poor prognosis among ccRCC patients. METTL14 augments the expression of FDX1 by enhancing the stability of the FDX1 messenger RNA. METTL14 upregulates FDX1 expression and consequently enhances cuproptosis in ccRCC cells. Methyltransferase METTL14 preserves the stability of FDX1 messenger RNA via m6A modification of FDX1 messenger RNA and acts as a crucial mediator of cuproptosis. Nevertheless, in clear cell renal cell carcinoma (ccRCC), the level of cuproptosis declines as a result of the diminished expression of these two factors, and the proliferation capabilities of ccRCC cells are augmented.
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