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, invivo 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.
Highlights
Hepatocellular carcinoma (HCC) is the most common malignant tumor type of the liver and originates from the malignant transformation of hepatocytes; it accounted for 75‐85% of primary liver cancers in 2018 worldwide [1,2]
nuclear enriched abundant transcript 1 (NEAT1) expression was detected in the HCC cell lines Hep3B, SNU‐449, SNU‐398, Huh7, and MHCC‐97H, the hepatoblastoma cell line Huh6 and the hepatic stellate cell line LX‐2
The EdU assay was performed, which verified that Huh7 and MHCC‐97H cell proliferation was significantly suppressed by reduced NEAT1 expression and significantly induced by the upregulation of NEAT1 (Fig. 2E and F)
Summary
Hepatocellular carcinoma (HCC) is the most common malignant tumor type of the liver and originates from the malignant transformation of hepatocytes; it accounted for 75‐85% of primary liver cancers in 2018 worldwide [1,2]. MicroRNAs (miRNAs) are a class of evolutionarily conservative non‐coding RNAs comprised of ~22 nucleotides that have an essential role in posttranscriptional gene regulation [7] They can bind to numerous sites (nucleotides 2‐7), those in the 3'‐untranslated region of target gene mRNAs, and modulate target gene expression by suppressing the translation of target mRNAs [8]. Both lncRNAs and miRNAs serve key roles in numerous biological processes, including the immune response, cell growth, epigenetic regulation, tumorigenesis and cell differentiation [9,10]. The lncRNA CASC2 regulates the development of HCC cells via the miR‐362‐5p/NF‐κB axis [15]
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