LncRNA SNHG12 promotes proliferation and migration of hepatic progenitor cells via the Wnt/β-catenin pathway.

Abstract

Hepatic progenitor cells (HPCs) play an important role in the treatment of chronic liver disease. To investigate the effect and mechanism of long noncoding RNAs/small nucleolar RNA host gene 12 (lncRNA SNHG12) on the proliferation and migration of the HPC cell line WB-F344. Hepatic progenitor cells were divided into a no-treatment group (sham), empty vector transfection of plasmid pcDNA3.1 (NC vector), pcDNA3.1-SNHG12 (SNHG12), negative short hairpin RNA (sh-NC), SNHG12 shRNA (sh-SNHG12), and pcDNA3.1-SNHG12+salinomycin intervention (SNHG12+salinomycin) groups. Cell proliferation, cell cycle and migration ability, as well as albumin (ALB), alpha-fetoprotein (AFP), â-catenin, cyclin D1, and c-Myc protein expression in each group were determined using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell migration assays, enzyme-linked immunosorbent assay (ELISA), and western blot. The overexpression of lncRNA SNHG12 significantly upregulated proliferation, migration and cell cycle progression of WB-F344 cells. Furthermore, the overexpression of lncRNA SNHG12 increased the level of ALB, and the protein expression of â-catenin, cyclin D1 and c-Myc in the cell line, while decreasing the level of AFP. Conversely, the knockdown of lncRNA SNHG12 displayed the opposite effects. The inhibition of the Wnt/â-catenin signaling pathway with salinomycin significantly downregulated the â-catenin, cyclin D1 and c-Myc protein expression in WB-F344 cells. The lncRNA SNHG12 promotes the proliferation and migration of WB-F344 cells via activating the Wnt/â-catenin pathway.