Hypoxia is considered a critical contributor to renal cell carcinoma progression, including invasion and metastasis. However, the potential mechanisms by which it promotes invasion and metastasis have not yet been clarified. The purpose of this study was to investigate the role and mechanism of hypoxia-induced renal cell carcinoma and provide evidence-based medical proof for improvements to postoperative nursing of renal cell carcinoma patients. A total of 64 patients with renal cell carcinoma were divided into the observation group (nursing based on oxygen administration) and the control group (conventional nursing). Renal function indexes, serum inflammatory factors, and tumor markers were evaluated. The human renal cell carcinoma cell line A498 under hypoxia/normoxia was used as an experimental model in vitro and the biological characteristics and mitochondrial function of the cells were assessed. Nursing based on oxygen administration decreased the value of renal function indexes, serum inflammatory factors, and tumor markers in renal cell carcinoma patients. Hypoxia was found to induce A498 cell invasion, migration, and the release of inflammatory cytokines, while repressing human solute carrier family 14 member 1 gene expression. Elevated levels of solute carrier family 14 member 1 expression induced mitochondrial reactive oxygen species accumulation, diminished the intracellular adenosine triphosphate level, and destroyed both mitochondrial membrane potential integrity and mitochondrial morphology. Overexpression of the solute carrier family 14 member 1 gene could abolish hypoxia-induced invasion, reduce the migration of A498 cells, inhibit the hypoxia-induced release of inflammatory cytokines, and arrest the cell cycle at the G1/S checkpoint. These data reveal that nursing based on oxygen administration can improve the clinical efficacy of renal cell carcinoma therapies, being safe and effective. The results elucidate a mechanism wherein the solute carrier family 14 member 1 gene participates in the occurrence and development of hypoxia-induced renal cell carcinoma in a mitochondria-dependent manner.

中文翻译：

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人溶质载体家族14成员1基因在缺氧肾癌发生中的作用及其对肿瘤护理的启示

缺氧被认为是肾细胞癌进展（包括侵袭和转移）的关键因素。然而，其促进侵袭和转移的潜在机制尚未阐明。本研究旨在探讨低氧诱导肾细胞癌的作用及机制，为改善肾细胞癌术后护理提供循证医学依据。将64例肾细胞癌患者分为观察组(以给氧为主的护理)和对照组(常规护理)。评估肾功能指标、血清炎症因子和肿瘤标志物。以缺氧/常氧条件下的人肾癌细胞系A498为体外实验模型，评估细胞的生物学特性和线粒体功能。以给氧为主的护理降低了肾细胞癌患者的肾功能指标、血清炎症因子和肿瘤标志物的值。发现缺氧会诱导 A498 细胞侵袭、迁移和炎性细胞因子的释放，同时抑制人类溶质载体家族 14 成员 1 基因的表达。溶质载体家族 14 成员 1 表达水平升高诱导线粒体活性氧积累，降低细胞内三磷酸腺苷水平，并破坏线粒体膜电位完整性和线粒体形态。溶质载体家族14成员1基因的过表达可以消除缺氧诱导的侵袭，减少A498细胞的迁移，抑制缺氧诱导的炎性细胞因子释放，并将细胞周期停滞在G1 / S检查点。这些数据表明以给氧为主的护理可以提高肾细胞癌治疗的临床疗效，且安全有效。结果阐明了溶质载体家族14成员1基因以线粒体依赖的方式参与缺氧肾癌发生发展的机制。这些数据表明以给氧为主的护理可以提高肾细胞癌治疗的临床疗效，且安全有效。结果阐明了溶质载体家族14成员1基因以线粒体依赖的方式参与缺氧肾癌发生发展的机制。这些数据表明以给氧为主的护理可以提高肾细胞癌治疗的临床疗效，且安全有效。结果阐明了溶质载体家族14成员1基因以线粒体依赖的方式参与缺氧肾癌发生发展的机制。