miR-222 enhances HBx-HepG2 cell growth via regulation of BCL2L13 gene

AIM: To investigate the regulation of miR-222 on BCL2L13 gene and its effect on the growth and apoptosis of HBx-HepG2 cells, and to explore the underlying molecular mechanisms. METHODS: The expression level of miR-222 was detected by RT-qPCR. The HBx-HepG2 cell growth was examined by MTT and colony formation assays. The cell cycle and apoptosis were analyzed by flow cytometry. The recombination vector pmirGLO-BCL2L13 was constructed, and dual-luciferase reporter experiment was performed to validate the target of miR-222. RESULTS: The expression level of miR-222 in the HBx-HepG2 cells was significantly higher than that in the L02 cells (P<0.05). Over-expression of miR-222 enhanced HBx-HepG2 cell growth, changed cell cycle, and inhibited apoptosis (P<0.05). Knockdown of miR-222 reduced HBx-HepG2 cell growth, changed cell cycle, and increased cell apoptotic rate (P<0.05). BCL2L13 was down-regulated in the HBx-HepG2 cells as compared with L02 cells (P<0.05), and knockdown of miR-222 in the HBx-HepG2 cells increased the expression level of BCL2L13 (P<0.05). The results of dual-luciferase reporter assay and restore experiment showed that miR-222 negatively regulated the expression of BCL2L13 via targeting 3'UTR of BCL2L13, resulting in the promotion of HBx-HepG2 cell growth. CONCLUSION: miR-222 enhances HBx-HepG2 cell growth via down-regulation of BCL2L13.