透明细胞肾细胞癌中铜增生的关键调控因子铁氧化还原蛋白1与预后和免疫细胞浸润相关

Dian Xia, Kun Liu, Wen Jiao, Longfei Peng, Qi Liu, Chang Liu, Liangkuan Bi
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引用次数: 0

摘要

多项研究表明,透明细胞肾细胞癌(clear cell renal cell carcinoma, ccRCC)作为膀胱最常见的恶性肿瘤之一,其发生和发展可能与代谢和免疫机制密不可分。最近发现的cuprotosis揭示了一种基于线粒体呼吸和三羧酸循环的新的细胞死亡机制,并且cuprotosis与代谢过程密切相关。铜下垂过程不同于以往发现的细胞死亡过程如焦亡、凋亡和铁下垂,有望为肿瘤机制的研究提供新的视角。在这里,我们的目的是利用生物信息学和实验验证相结合的方法来探索铜肾增生的关键调节因子在肾癌中的重要作用。我们发现铁氧还蛋白1 (FDX1)与ccRCC肿瘤微环境中多种免疫细胞的浸润及免疫治疗应答有关。同时,实验证实FDX1在ccRCC中显著降低,这与之前的分析结果一致。综上所述,FDX1有望成为ccRCC免疫浸润、免疫治疗和肿瘤预后的重要标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ferredoxin 1, the key regulator of cuproptosis, was associated with prognosis and immune cell infiltration in clear cell renal cell carcinoma

Ferredoxin 1, the key regulator of cuproptosis, was associated with prognosis and immune cell infiltration in clear cell renal cell carcinoma

According to a number of studies, the occurrence and progression clear cell renal cell carcinoma (ccRCC), among the most prevalent cancerous tumors of the urinary bladder, may be inextricable from metabolism and immunology. The recent discovery of cuproptosis revealed a novel cell death mechanism based on mitochondrial respiration and the tricarboxylic acid cycle, and cuproptosis is strongly linked to the metabolic process. The cuproptosis process is different from the previously revealed cell death processes such as pyroptosis, apoptosis and ferroptosis, which is expected to provide a new perspective in the study of tumor mechanism. Here we aim to explore the important role of key regulators of cuproptosis in renal cancer using a combination of bioinformatics and experimental validation. We found that Ferredoxin 1 (FDX1) was related to the infiltration of various immune cells in the tumor microenvironment and the response to immunotherapy in ccRCC. At the same time, the experiment confirmed that FDX1 was significantly lower in ccRCC, which was consistent with the previous analysis results. In conclusions, FDX1 was expected to be an important marker of immune infiltration, immunotherapy, and tumor prognosis in ccRCC.

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