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SLC12A8 促进非小细胞肺癌(NSCLC)细胞的迁移和侵袭。

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

机构信息

Department of the First Respiratory, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, China.

Department of Endocrinology, Second Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, China.

出版信息

Gen Physiol Biophys. 2024 Sep;43(5):445-455. doi: 10.4149/gpb_2024020.

DOI:10.4149/gpb_2024020
PMID:39140681
Abstract

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.

摘要

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-间充质转化(EMT)的影响。使用 GEPIA 数据库检测 SLC12A8 在肺癌细胞中的表达模式。随后,通过 qRT-PCR 和 Western blot 分析检测 NSCLC 组织和细胞系中 SLC12A8 的表达。通过 Kaplan-Meier 图和单因素及多因素 COX 回归曲线评估 NSCLC 患者的总体预后。使用慢病毒介导的 shRNA 在 A549 和 H1299 细胞中建立 SLC12A8 的敲低模型。通过 CCK-8 测定、Transwell 和流式细胞术分别评估细胞增殖、侵袭、迁移和凋亡。Western blot 分析用于测量 EMT 相关蛋白(E-钙粘蛋白和波形蛋白)的表达水平。SLC12A8 的表达水平在 NSCLC 细胞系和组织中均显著升高。高 SLC12A8 表达与 NSCLC 患者预后不良相关。敲低 SLC12A8 导致 NSCLC 细胞增殖、迁移和侵袭能力显著下降,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,E-钙粘蛋白表达增加。结果表明,降低 SLC12A8 表达可能抑制 NSCLC 细胞的恶性表型和 EMT。SLC12A8 可能成为 NSCLC 进展临床管理的靶点。

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