LncRNA SNHG15 promotes proliferation, migration and invasion of lung adenocarcinoma cells by regulating COX6B1 through sponge adsorption of miR-30b-3p.
10.12122/j.issn.1673-4254.2025.07.16
- Author:
Xiuying GONG
1
;
Shunfu HOU
1
;
Miaomiao ZHAO
1
;
Xiaona WANG
1
;
Zhihan ZHANG
2
;
Qinghua LIU
1
;
Chonggao YIN
3
;
Hongli LI
1
Author Information
1. School of Basic Medical Sciences, Shandong Second Medical University, Weifang 261000, China.
2. School of Life Sciences and Technology, Shandong Second Medical University, Weifang 261000, China.
3. School of Nursing, Shandong Second Medical University, Weifang 261000, China.
- Publication Type:Journal Article
- Keywords:
COX6B1;
invasion;
long non-coding RNA SNHG15;
lung adenocarcinoma;
miR-30b-3p;
migration
- MeSH:
Humans;
MicroRNAs/metabolism*;
RNA, Long Noncoding/genetics*;
Cell Proliferation;
Cell Movement;
Lung Neoplasms/genetics*;
Adenocarcinoma of Lung;
Neoplasm Invasiveness;
A549 Cells;
Adenocarcinoma/genetics*;
Gene Expression Regulation, Neoplastic;
Cell Line, Tumor
- From:
Journal of Southern Medical University
2025;45(7):1498-1505
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells.
METHODS:The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both.
RESULTS:LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (r=0.128, P=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown.
CONCLUSIONS:LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.
