低氧被认为是肾细胞癌进展，包括侵袭和转移的一个重要因素。然而，它促进侵袭和转移的潜在机制尚未被证实。本研究的目的是探讨低氧引起的肾细胞癌的作用和机制，并提供基于证据的医学证明，以改善肾细胞癌患者的术后护理。64名肾细胞癌患者被分为观察组（基于氧气治疗的护理）和对照组（传统护理）。评估肾功能指标，血清炎症因子和肿瘤标志物。使用低氧 / 正氧作为人肾细胞癌细胞系A498的实验模型，并评估细胞的生物学特性和线粒体功能。基于氧气治疗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水平。发现低氧诱导A498细胞侵袭，迁移和炎性细胞因子的释放，同时抑制人溶质载体家族14成员1基因的表达。溶质载体家族14成员1表达升高诱导线粒体反应性氧化物积累，降低细胞内腺苷酸三磷酸水平，并破坏线粒体膜电位完整性和线粒体形态。过表达溶质载体家族14成员1基因可以消除低氧诱导的侵袭，减少A498细胞的迁移，抑制低氧诱导的炎性细胞因子的释放，并阻滞细胞周期在G1/S检查点。 这些数据表明，基于氧气治疗的护理可提高肾细胞癌治疗的临床疗效，安全有效。结果阐明了一种机制，即溶质载体家族14成员1基因以线粒体依赖的方式参与低氧诱导的肾细胞癌的发生和发展。 © 2023. The Author(s).

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.© 2023. The Author(s).