METTL14-mediated FDX1 m6A methylation inhibited the proliferation of clear cell renal cell carcinoma.
5 affiliations
- 1Department of Urology, Tianjin First Central Hospital, Tianjin Medical University, Tianjin, China.
- 2Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, China.
- 3Shunde Hospital of Southern Medical University, Guangdong, China.
- 4Department of Urology, Tianjin First Central Hospital, Tianjin Medical University, Tianjin, China. [email protected].
- 5Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, China. [email protected].
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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BibTeX
@article{bai2026mettl14mediated,
title = {{METTL14-mediated FDX1 m6A methylation inhibited the proliferation of clear cell renal cell carcinoma.}},
author = {Zhijie Bai and Chun Wang and Junlin Shen and Yanjie Yang and Qian Liu and Zhiqun Shang},
journal = {Medical oncology (Northwood, London, England)},
year = {2026},
month = oct,
doi = {10.1007/s12032-026-03438-9},
url = {https://europepmc.org/article/MED/42900269},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - METTL14-mediated FDX1 m6A methylation inhibited the proliferation of clear cell renal cell carcinoma.
AU - Zhijie Bai
AU - Chun Wang
AU - Junlin Shen
AU - Yanjie Yang
AU - Qian Liu
AU - Zhiqun Shang
PY - 2026
DA - 2026/10/20
JO - Medical oncology (Northwood, London, England)
DO - 10.1007/s12032-026-03438-9
UR - https://europepmc.org/article/MED/42900269
AB - 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.
SN - 1357-0560
SN - 1559-131X
ER -