Silencing of microRNA-210 inhibits the progression of liver cancer and hepatitis B virus-associated liver cancer via targeting EGR3.

Background: This study was aimed to investigate the regulatory role of microRNA-210 (miRNA-210) on the progression of liver cancer and Hepatitis B virus (HBV)-associated liver cancer.

Methods: The expression of miRNA-210 was detected in liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells by qRT-PCR. MiRNA-210 was silenced in HepG2 and HepG2.2.15 cells by the transfection of miRNA-210 inhibitor. The cell viability and apoptosis was detected by MTT assay and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression of EGR3 was detected by Western blot. The regulatory relationship between EGR3 and miRNA-210 was predicted by TargetScan and identified by Dual luciferase reporter gene assay.

Results: MiRNA-210 was overexpressed in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 inhibited the viability and promoted the apoptosis of HepG2 and HepG2.2.15 cells (P < 0.05). EGR3 was a target of miRNA-210, which was down-regulated in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 increased the mRNA and protein expression of EGR3 (P < 0.05). Silencing of EGR3 reversed the anti-tumor effect of miRNA-210 inhibitor on HepG2 and HepG2.2.15 cells (P < 0.05).

Conclusions: Silencing of miRNA-210 inhibits the progression of liver cancer and HBV-associated liver cancer via up-regulating EGR3.