Silencing LINC01116 suppresses the development of lung adenocarcinoma via the AKT signaling pathway

Abstract Background A growing body of evidence has proven that long noncoding ribonucleic acids (lncRNAs) are important epigenetic regulators that play crucial parts in the pathogenesis of human cancers. Previous studies have shown that long intergenic nonprotein coding RNA 01116 (LINC01116) is a carcinogen in several carcinomas; however, its function in lung adenocarcinoma (LUAD) has not been clarified. Here, we aimed to investigate the role of LINC01116 in LUAD. Methods The relative expression levels of LINC01116 in LUAD cell lines and tissues were detected by quantitative reverse transcription polymerase chain reaction. A Kaplan–Meier survival analysis was performed using patient information from the Gene Expression Profiling Interactive Analysis (GEPIA) database. LUAD proliferation, invasion, migration, and apoptosis were measured by performing cell counting kit‐8, colony formation, transwell, wound healing, and flow cytometric assays. A xenograft animal experiment was performed to investigate the effect of LINC01116 in vivo. Protein kinase B (AKT) signaling pathway‐related protein expressions were tested by Western blot assay. Results LINC01116 expression was upregulated in LUAD cells and tissues. The loss‐of‐function experiments on LUAD cells revealed that silencing LINC01116 expression could decrease cell viability both in vitro and in vivo. Furthermore, silencing LINC01116 inhibited LUAD cell invasion and migration and induced cell apoptosis. Mechanically, silencing LINC01116 significantly decreased p‐AKT protein levels, and an AKT pathway stimulator could rescue the suppressive effects of small interfering LINC011116‐specific RNAs on LUAD development. Conclusions Our study demonstrated that silencing LINC01116 suppresses the development of LUAD via the AKT signaling pathway