MicroRNA-106a-5p promotes the proliferation, autophagy and migration of lung adenocarcinoma cells by targeting LKB1/AMPK.

It has previously been reported that lung cancer has the highest morbidity and mortality rate worldwide; however, the pathogenesis underlying lung cancer has not been fully elucidated. The aim of the present was primarily to assess the influence of microRNA (miR)-106a-5p on the biological behaviors of lung cancer cells. In the present study, bioinformatics analysis was used to analyze the expression characteristics of miR-106a-5p and its relationship with the prognosis of patients with lung adenocarcinoma (LUAD) in The Cancer Genome Atlas. A dual luciferase reporter assay was performed to verify the binding of miR-106a-5p and liver kinase B1 (LKB1). The Cell Counting Kit-8, colony formation and Transwell assays were utilized to detect cell viability, proliferation and migration, respectively. Protein and RNA expression levels were examined by western blotting and reverse transcription-quantitative PCR analysis, respectively. It was observed that miR-106a-5p was highly expressed in LUAD and associated with poor prognosis. miR-106a-5p promoted the proliferation and migration of LUAD cells, and inhibited autophagy. By contrast, LKB1 inhibited cell proliferation and migration, promoted autophagy and blocked the cancer-promoting effects of miR-106a-5p. Overexpression of miR-106a-5p inhibited the phosphorylation of AMP-activated protein kinase (AMPK) and tuberin (TSC2), and promoted the phosphorylation of mTOR. By contrast, overexpression of LKB1 blocked the promotion of mTOR phosphorylation, and the inhibition of AMPK and TSC2 phosphorylation caused by miR-106a-5p. In summary, the results of the present study indicated that miR-106a-5p regulated the phosphorylation of the AMPK pathway by targeting LKB1, and was involved in the proliferation, migration and autophagy of LUAD cells.