基因沉默
肺癌
癌基因
免疫印迹
癌症研究
细胞凋亡
下调和上调
细胞生长
癌症
荧光素酶
靶向治疗
小RNA
生物
医学
细胞培养
转染
肿瘤科
基因
细胞周期
内科学
生物化学
遗传学
作者
Zhibin Lu,Zhichao Xiao,Qi Wang,Chunfeng Pan,Yang Xia,Weibing Wu,Liang Chen
出处
期刊:Cancer Biomarkers
[IOS Press]
日期:2023-09-15
卷期号:38 (3): 379-391
摘要
BACKGROUND: Non-small lung cancer ranks first in the cancer-related death of all malignant tumors. Exploring novel biological targets is of great significance for diagnosis and therapy of NSCLC. OBJECTIVE: In this study, we aimed to explore the effect of LINC00668 on the biological functions of NSCLC cells and the underlying mechanism. METHODS: RT-qPCR assays and western blot assays were utilized to estimate the relative gene expression at mRNA and protein levels, respectively. CCK8, colony formation, wound healing, transwell, and cell apoptosis assays were employed to assess cell function. IHC and FISH assays were used to determine the gene expression in NSCLC tissues. RIP and dual-luciferase assays were conducted to validate the combination between LINC00668 and miR-518c-3p. The correlation of expression between miR-518c-3p and LINC00668 or TRIP4 was determined by Pearson correlation analysis. RESULTS: LINC00668 was aberrantly upregulated in NSCLC tumor tissues and cell lines. Inhibition of LINC00668 significantly suppressed tumor proliferation, migration, invasion and promoted cell apoptosis. Mechanistically, LINC00668 could bind to miR-518c-3p, thus targeting the 3’UTR of TRIP4. TRIP4 overexpression rescued the weakened cell function mediated by LINC00668 silencing. CONCLUSIONS: LINC00668 acted as an oncogene in NSCLC progression through miR-518c-3p/TRIP4 axis. Our study disclosed a new mechanism of LINC00668 functioned in NSCLC and may give a deeper insight of the targeted therapy of NSCLC in the future.
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