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.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
飞快的邴完成签到,获得积分10
1秒前
1秒前
1秒前
1秒前
2秒前
炙热忆文发布了新的文献求助30
2秒前
3秒前
烟花应助研小白采纳,获得10
5秒前
5秒前
哈哈哈哈发布了新的文献求助10
6秒前
6秒前
onmyway完成签到,获得积分10
6秒前
星空发布了新的文献求助10
6秒前
纯真镜子发布了新的文献求助10
7秒前
Gauss应助Markov采纳,获得30
7秒前
2211完成签到 ,获得积分10
7秒前
7秒前
乔乔兔发布了新的文献求助10
8秒前
易天完成签到,获得积分20
8秒前
8秒前
8秒前
9秒前
10秒前
10秒前
Hanoi347发布了新的文献求助50
11秒前
11秒前
炙热忆文完成签到,获得积分10
11秒前
解语花031发布了新的文献求助10
11秒前
天天快乐应助从容水蓝采纳,获得10
12秒前
12秒前
张美发布了新的文献求助10
12秒前
Ava应助wxy采纳,获得10
12秒前
科研通AI2S应助wf采纳,获得10
13秒前
科研小石发布了新的文献求助10
13秒前
14秒前
AA发布了新的文献求助10
14秒前
土豆宝发布了新的文献求助30
14秒前
15秒前
乔乔兔完成签到,获得积分10
15秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Aerospace Standards Index - 2026 ASIN2026 2000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Social Cognition: Understanding People and Events 1000
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6031851
求助须知:如何正确求助?哪些是违规求助? 7715845
关于积分的说明 16198144
捐赠科研通 5178603
什么是DOI,文献DOI怎么找? 2771389
邀请新用户注册赠送积分活动 1754681
关于科研通互助平台的介绍 1639737