Foundation of ceRNA networks and functional validation of AFAP1-AS1 in lung adenocarcinoma
- VernacularTitle:肺腺癌ceRNA调控网络构建及AFAP1-AS1功能验证
- Author:
Huixin WANG
1
;
Qian LI
1
;
Xiaowen HOU
1
;
Xinzhu SHI
2
;
Xu FENG
1
Author Information
1. Statistics Teaching and Research Office of the School of Public Health, Shenyang Medical College, Shenyang, 110034, P. R. China
2. Epidemiology Teaching and Research Office of the School of Public Health, Shenyang Medical College, Shenyang, 110034, P. R. China
- Publication Type:Journal Article
- Keywords:
Bioinformatics;
lung adenocarcinoma;
competing endogenous RNA;
long non-coding RNA;
AFAP1-AS1
- From:
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery
2024;31(04):576-584
- CountryChina
- Language:Chinese
-
Abstract:
Objective A competing endogenous RNA (ceRNA) regulatory network associated with long non-coding RNA (lncRNA) specific for lung adenocarcinoma (LUAD) was constructed based on bioinformatics methods, and the functional mechanism of actinfilament-associated protein 1-antisense RNA1 (AFAP1-AS1) in LUAD was analyzed, in order to provide a new direction for the study of LUAD therapeutic targets. Methods The gene chip of LUAD was downloaded from the Gene Expression Omnibus (GEO), and lncRNA and mRNA with differential expression between LUAD and normal tissues were screened using GEO2R online software, and their target genes were predicted by online databases to construct ceRNA networks and perform enrichment analysis. In cell experiments, AFAP1-AS1 was genetically knocked down and siRNA was constructed and transfected into LUAD cells A549 by cell transfection. CCK8, transwell, scratch assay and flow cytometry were used to detect the ability of cells to proliferate, invade, migrate and apoptosis. Results A total of 6 differentially expressed lncRNA and 494 differentially expressed mRNA were identified in the microarray of LUAD. The ceRNA network involved a total of 6 lncRNA, 22 miRNA, and 55 mRNA. Enrichment analysis revealed that mRNA was associated with cancer-related pathways. In cell assays, knockdown of AFAP1-AS1 inhibited cell proliferation, invasion, and migration, and AFAP1-AS1 promoted apoptosis. Conclusion In this study, we construct a lncRNA-mediated ceRNA network, which may help to further investigate the mechanism of action of LUAD. In addition, through cellular experiments, AFAP1-AS1 is found to have potential as a therapeutic target for LUAD.
