Downregulation of MiR-93 Expression Reduces Cell Proliferation and Clonogenicity of HepG2 Cells

Background/Aims: MiR-93 was observed in various types of cancers. This study is to investigate a role of miR-93 in the carcinogenesis of HCC. Methodology: The expression of miR-93 in HepG2 cells and primary human hepatocytes (PHHC) was measured by RT-PCR. HepG2 cells were transfected with miR-93 inhibitor or negative control. The cell proliferation was determined by using the CellTiter 96 (R) Aqueous One Solution Cell Proliferation Assay kit. The migration and clonogenicity in vitro were measured by cell migration assay, colony formation analysis and anchorage-independent growth assay. The apoptosis and cell cycle were detected by flow cytometry analysis. The mRNA and protein levels of transforming growth factor-beta type II receptor (TGFBR2) and integrin beta8 (ITGB8) were evaluated by RT-PCR and western blot analysis. Results: MiR-93 was upregulated in HepG2 cells compared with PHHC and inhibition of miR-93 significantly suppressed HepG2 cell proliferation, migration and colony formation. The expressions of TGFBR2 and ITGB8 were upregulated when miR-93 was inhibited. Conclusions: Our results reveal an important contribution for miR-93 in hepatocarcinogenesis and suggest a role for TGFBR2 and ITGB8 dysregulation in this process. Thus, the use of synthetic inhibitor of miR-93 may prove to be a promising approach to liver cancer treatment.