Abstract
Long non‑coding RNAs (lncRNAs) serve a pivotal role in hepatocellular carcinoma (HCC) progression and have been confirmed to participate in the carcinogenesis and development of HCC. Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationship between lncRNA NEAT1 and HCC remains unclear. The present study found that NEAT1 was significantly overexpressed in HCC cell lines compared with LX‑2 hepatic stellate cells. NEAT1 expression in Huh7 and MHCC‑97H cells was increased following transfection with lentivirus (LV)‑NEAT1 but inhibited by LV‑short hairpin NEAT1. Knockdown of NEAT1 significantly repressed HCC cell viability, increased cell apoptosis, and inhibited cell migration and invasion capacity. By contrast, upregulation of NEAT1 demonstrated the reverse effects. Furthermore, microRNA‑320a (miR‑230a) was predicted to be a direct target of NEAT1 and was significantly reduced in HCC cells. Additionally, a luciferase activity reporter assay and RNA immunoprecipitation assay were performed to confirm the interaction between miR‑320a and NEAT1. Using a dual‑luciferase activity assay, L antigen family member 3 (LAGE3) was found to be a target of miR‑320a. Finally, in vivo nude mouse models were established, and the results indicated that NEAT1 suppressed HCC progression by targeting miR‑320a. In conclusion, the present findings revealed that the NEAT1/miR‑320a/LAGE3 axis participates in HCC development and that NEAT1 could be used as a biomarker for HCC.