LINC02535/miR-30b/CCNA2 axis participates in the pathogensis of lung adenocarcinoma by inhibiting apoptosis and promoting proliferation

Objective To explore the role of the LINC02535/miR-30b/CCNA2 axis in the pathogenesis of lung adenocarcinoma (LUAD), and identify relevant molecular markers and signaling pathways by analyzing gene expression and verify their effects.Methods The gene expression profiles of lncRNA, miRNA, and mRNA in LUAD and related clinical data were obtained from the Cancer Genome Atlas (TCGA), and differentially expressed genes were screened using the "edgeR" differential analysis package in R3.6.0 software. Furthermore, weighted gene co-expression network analysis was performed using the "WGCNA" package in R3.6.0 software to establish a gene co-expression network map of ceRNA. Meanwhile, two human LUAD cell lines A549 and H1299 and one standard bronchial epithelial cell line (BEAS-2B) were cultivated for transfection. Cell proliferation was evaluated by qRT-PCR, CCK-8 assay, EdU assay, and cell cycle analysis.Results From the TCGA database, high-expression lncRNAs, low-expression miRNAs, and high-expression mRNAs were obtained. Through weighted gene co-expression network analysis, 20 lncRNAs with significant differences in survival analysis were screened out. Among them, LINC02535 showed a significant negative correlation with miR-30b, with binding targets. Further research found that LINC02535 was overexpressed in LUAD tissues and cell lines, while miR-30b was significantly down-regulated. Reduced expression of LINC02535 resulted in inhibitory effect on cell proliferation, cell apoptosis and G1 to S phase transition. Meanwhile, down-regulation of LINC02535 led to increased expression of miR-30b, and then decreased the expression of CCNA2.Conclusions The LINC02535/miR-30b/CCNA2 axis participates in the pathogenesis of LUAD by inhibiting apoptosis and promoting proliferation, which may become a potential molecular target for treating LUAD.