MicroRNA-421 promotes the progression of non-small cell lung cancer by targeting HOPX and regulating the Wnt/β-catenin signaling pathway

MicroRNAs (miRNAs) function as key regulators of numerous types of cancers. miRNA (miR)-421 expression is dysregulated in a variety of tumors; however, its role in non-small cell lung cancer (NSCLC) remains unclear. In the present study, the role and molecular mechanism of miR-421 in NSCLC was investigated. In this study, miRNA (miR)-421 was upregulated in NSCLC tissues and cell lines used the reverse transcriptase quantitative polymerase chain reaction. Ectopic expression of miR-421 significantly promoted cell proliferation in vitro and tumor growth in vivo by promoting cell cycle progression via CCK-8, colony formation, EdU assay, xenograft model and cell cycle assay. In addition, miR-421 inhibited NSCLC cell apoptosis by flow cytometry apoptosis assay, as evidenced by anti-apoptosis gene Bcl-2 and apoptosis gene cleaved caspase-3 and cleaved PARP using western blot assay. Furthermore, miR-421 promoted cell migration and invasion through EMT process using Transwell and western blot assay. It was also demonstrated that miR-421 can directly target HOPX by the EGFP reporter assay and western blot assay. MiR-421 overexpression promoted the protein expression levels of β-catenin, cyclin D1 and c-myc by western blot assay, which are the downstream genes of Wnt pathway. These data indicated that miR-421 may act as an oncogene through the effects of HOPX on the Wnt/β-catenin signaling pathway and may provide insight into the mechanisms underlying carcinogenesis and the identification of potential biomarkers associated with NSCLC.