本研究旨在探讨SLC12A8对非小细胞肺癌（NSCLC）细胞侵袭、迁移和上皮间质转化（EMT）的影响。采用GEPIA数据库检查肺癌细胞中SLC12A8的表达模式。随后，进行 qRT-PCR 和蛋白质印迹分析以评估 NSCLC 组织和细胞系中的 SLC12A8 表达。使用Kaplan-Meier图以及单变量和多变量COX回归曲线评估NSCLC患者的总体预后。在 A549 和 H1299 细胞中使用慢病毒介导的 shRNA 建立了 SLC12A8 的敲低。分别使用CCK-8测定、transwell和流式细胞术技术评估细胞增殖、侵袭、迁移和凋亡。进行蛋白质印迹分析以测量 EMT 相关蛋白（E-钙粘蛋白和波形蛋白）的表达水平。发现 SLC12A8 的表达水平在 NSCLC 细胞系和组织中显着较高。 SLC12A8 高表达与 NSCLC 患者的不良预后相关。敲除SLC12A8会导致NSCLC细胞的增殖、迁移和侵袭能力显着下降，同时促进细胞凋亡。此外，SLC12A8 敲低导致 N-钙粘蛋白和波形蛋白水平降低，同时 E-钙粘蛋白表达增加。结果表明，减少SLC12A8的表达可能会抑制NSCLC细胞的恶性表型以及EMT。 SLC12A8 可作为 NSCLC 进展临床管理的靶点。

This study aims to investigate the impacts of SLC12A8 on the invasion, migration, and epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) cells. GEPIA database was employed to examine SLC12A8 expression pattern in lung cancer cells. Subsequently, qRT-PCR and Western blot analyses were conducted to assess SLC12A8 expression in NSCLC tissues and cell lines. The overall prognosis of NSCLC patients was evaluated using Kaplan-Meier plot and univariate and multivariate COX regression curves. The knockdown of SLC12A8 was established using lentivirus-mediated shRNA in A549 and H1299 cells. Cell proliferation, invasion, migration, and apoptosis were evaluated using CCK-8 assay, transwell, and flow cytometry techniques, respectively. Western blot analysis was performed to measure the expression levels of EMT-related proteins (E-cadherin and vimentin). The expression level of SLC12A8 was found to be significantly higher in both NSCLC cell lines and tissues. High SLC12A8 expression was correlated with a poor prognosis in NSCLC patients. Knocking down SLC12A8 led to a significant decrease in proliferation, migration, and invasion abilities, while promoting apoptosis in NSCLC cells. Additionally, SLC12A8 knockdown resulted in decreased levels of N-cadherin and vimentin, along with increased E-cadherin expression. The results indicate that reducing SLC12A8 expression may suppress the malignant phenotype of NSCLC cells, as well as the EMT. SLC12A8 may serve as a target for the clinical management of NSCLC progression.