Abstract
Long non-coding RNAs (lncRNAs) have recently been demonstrated to serve crucial roles in various diseases including tumor initiation and progression. However, the role of the lncRNA MIR31HG in non-small cell lung cancer (NSCLC) was not well established. The present study demonstrated that MIR31HG was significantly increased in tumor tissues compared with adjacent normal tissues, and increased MIR31HG expression levels were associated with histological differentiation grade, lymph node metastasis and Tumor-node metastasis (TNM) stage in patients with NSCLC. Patients who had a higher MIR31HG expression level, were predicted a shorter over survival (OS) time. Using in vitro assays, the present study demonstrated that the downregulation of MIR31HG expression significantly inhibited cell proliferation and cell invasion abilities. Furthermore, it was identified that knockdown of MIR31HG expression suppressed the cell epithelial-mesenchymal transition (EMT) phenotype by reducing the expression levels of Twist1 and Vimentin, but also increased the expression level of E-cadherin in NSCLC cells. Furthermore, the results of the present study demonstrated that downregulated MIR31HG inhibited the Wnt/β-catenin signaling pathway by decreasing the expression of glycogen synthase kinase 3β (GSK3β) and β-catenin, but increasing the phosphorylated (p)-GSK3β expression in NSCLC cells. Together, these data demonstrated that MIR31HG could be identified as a poor prognostic biomarker and a novel therapeutic target for patients with NSCLC.