Conclusion
LncRNA SNHG20 accelerates HCC progression by the miR-5095/MBD1 axis, indicating lncRNA SNHG20 can be used as a biomarker for patients with HCC.
Methods
LncRNA SNHG20, miR-5095, and MBD1 gene levels were determined using reverse transcription qPCR (RT-qPCR). Huh-7 and HepG2 cell bioactivities were evaluated using the CCK-8 kit, EdU, flow cytometry, and wound-healing migration tests. To assess the metastasis of Huh-7 and HepG2 cells, a transwell assay was used. The amounts of invasion- and proliferation-associated proteins were determined using western blot. Using the miRDB (www.mirdb.org) software, the possible target genes of lncRNA and miRNA were predicted, and this prediction was then verified by a twofold luciferase reporter test. To determine the pathologic alteration and Ki67 level in tumor tissues, H&E staining and IHC were employed. TUNEL was conducted to assess the presence of apoptotic bodies in the tumor tissues.
Objective
Long non-coding RNAs (lncRNAs) may have a significant regulatory effect on the progression of hepatocellular carcinoma (HCC), according to recent data. This study aims to investigate how SNHG20, a small nucleolar RNA host gene, contributes to the development of HCC.
Results
lncRNA SNHG20 exhibited a high expression in HCC cells (P<0.01). LncRNA SNHG20 knockdown inhibited HCC cell metastasis (P<0.01) and accelerated apoptosis (P<0.01). LncRNA SNHG20 acted as a sponge of miR-5095 in HCC. In addition, miR-5095 overexpression inhibited HCC cell metastasis (P<0.01) and accelerated apoptosis (P<0.01); and miR-5095 negatively targeted MBD1. Furthermore, LncRNA SNHG20 regulated HCC progression through the miR-5095/MBD1 axis, and LncRNA SNHG20 knockdown inhibited HCC growth.