Identification of <scp>FDFT1</scp> as a potential biomarker associated with ferroptosis in <scp>ccRCC</scp>
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- Ruizhen Huang
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Chiyu Zhang
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Xing Wang
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Xin Zou
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Zhengjie Xiang
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Zewei Wang
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Bin Gui
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Tao Lin
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
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- Honglin Hu
- Department of Urology The Second Affiliated Hospital of Nanchang University Nanchang China
抄録
<jats:title>Abstract</jats:title><jats:p>Renal cell carcinoma (RCC) seriously threatens people's lives and health. The identification of some precise biomarkers during the process of RCC progression and the pathophysiologic procedure is critical for improving the diagnosis and management of RCC. Evidence suggests that ferroptosis may play a pivotal role in eradicating clear cell RCC (ccRCC, KIRC) tumor cells. We screened out the target prognostic ferroptosis‐associated genes and examined the functions of farnesyl‐diphosphate farnesyltransferase (FDFT1) in 786‐O cells by plasmid transfection. In our study, we identified FDFT1 as a potential marker correlating with ferroptosis in KIRC. Upregulated FDFT1 inhibited cell proliferation, migration, and invasion, and the underlying antitumor effects may occur via the AKT signaling pathway. Our study provides helpful evidence to study the complex physiopathology of KIRC.</jats:p>
収録刊行物
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- Cancer Medicine
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Cancer Medicine 11 (21), 3993-4004, 2022-03-24
Wiley