SLC12A8 promotes the migration and invasion of non-small cell lung cancer (NSCLC) cells

波形蛋白 基因敲除 癌症研究 上皮-间质转换 小发夹RNA 肺癌 细胞迁移 流式细胞术 细胞凋亡 免疫印迹 A549电池 生物 细胞生长 污渍 肿瘤科 细胞 癌症 医学 免疫组织化学 内科学 转移 免疫学 基因 生物化学 遗传学
作者
Jing Nie,Jing Wang
出处
期刊:General Physiology and Biophysics [AEPress]
卷期号:43 (05): 445-455
标识
DOI:10.4149/gpb_2024020
摘要

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.

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