人溶质载体家族14成员1基因在缺氧诱导肾癌发生中的作用及其对肿瘤护理的启示

IF 2.4 3区 生物学 Q4 CELL BIOLOGY BMC Molecular and Cell Biology Pub Date : 2023-03-18 DOI:10.1186/s12860-023-00473-6
Jing Shi, Ruili Sha, Xilan Yang
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摘要

背景:缺氧被认为是肾细胞癌进展的关键因素,包括侵袭和转移。然而,它促进侵袭和转移的潜在机制尚未明确。本研究旨在探讨缺氧诱导肾细胞癌的作用及机制,为改善肾细胞癌患者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、血清炎症因子及肿瘤标志物。以缺氧/常氧条件下的人肾细胞癌细胞株A498为实验模型,对细胞的生物学特性和线粒体功能进行了评价。结果:基于给氧的护理降低了肾癌患者的肾功能指标、血清炎症因子及肿瘤标志物的价值。缺氧可诱导A498细胞侵袭、迁移和炎症因子的释放,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,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基因可以消除缺氧诱导的侵袭,减少A498细胞的迁移,抑制缺氧诱导的炎症因子的释放,使细胞周期在G1/S检查点停滞。结论:以给氧为基础的护理可提高肾细胞癌治疗的临床疗效,安全有效。这些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诱导肾癌发生和发展的机制。
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Role of the human solute carrier family 14 member 1 gene in hypoxia-induced renal cell carcinoma occurrence and its enlightenment to cancer nursing.

Background: 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.

Results: 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.

Conclusions: 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.

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来源期刊
BMC Molecular and Cell Biology
BMC Molecular and Cell Biology Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
5.50
自引率
0.00%
发文量
46
审稿时长
27 weeks
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