Abstract
Although long noncoding RNAs (lncRNAs) in lung adenocarcinoma (LUAD) have been increasingly studied, LINC01426 has not been fully investigated in LUAD. The GEPIA database revealed that LINC01426 was upregulated in LUAD tissues. In our study, we further verified the significantly high expression of LINC01426 in LUAD tissues and cell lines. We also analyzed the LINC01426 expression level and LUAD clinical features and found that high LINC01426 expression was associated with tumor diameter; tumor, node, and metastases (TNM) staging; lymph node metastasis (LNM); and overall survival (OS) rate of LUAD patients. In vitro experiments revealed that suppression of LINC01426 could repress the proliferation, migration and invasion of LUAD cells. Then, the bioinformatic analysis revealed that there were binding domains between miR-125a-5p and the 3'-UTR of LINC01426. As revealed by dual-luciferase reporter gene experiment and RNA Binding Protein Immunoprecipitation (RIP) assay, miR-125a-5p could bind to LINC01426. Additionally, the results of qRT-PCR and Pearson's analysis respectively revealed that miR-125a-5p was slightly expressed in LUAD and its expression was negatively correlated with LINC01426. Moreover, casein kinase 2 alpha 1 (CSNK2A1) was predicted to bind to miR-125a-5p. CSNK2A1 expression was remarkably high in LUAD tissues, negatively associated with miR-125a-5p, and positively correlated with LINC01426. Subsequently, our results showed that CSNK2A1 enhanced the malignant progression of LUAD cells. Overall, our study revealed that LINC01426 might regulate the malignant phenotype of LUAD via the miR-125a-5p/CSNK2A1 axis.