MicroRNA‑130a (miR‑130a) has been reported to be downregulated in hepatocellular carcinoma (HCC). However, the roles and underlying tumor‑suppressive mechanisms of miR‑130a in the pathogenesis of HCC remain unclear. In the current study, reduced expression of miR‑130a was observed in tumor tissues of patients with HCC in addition to in four HCC cell lines, BEL‑7402, MHCC97H, HepG2 and Huh7. Results of methyl thiazolyl tetrazolium (MTT) assays identified decreased growth rates of MHCC97H and HepG2 cells transfected with miR‑130a mimics. The in vitro colony formation assays demonstrated that the number of colonies formed by cells transfected with miR‑130a mimics and cells transfected with miR‑130a inhibitors was lower and higher, respectively, than that formed by the cells transfected with miR‑negative control. In addition, it was identified that overexpression of miR‑130a reduced the migration and invasiveness of MHCC97H and HepG2 cells. Luciferase reporter assays demonstrated that miR‑130a directly targeted the 3'‑untranslated region of Rho‑kinase 2 (ROCK2) mRNA. Northern and western blot analyses indicated that miR‑130a could modulate the mRNA and protein expression of ROCK2. Additionally, small‑interfering RNA‑mediated knockdown of ROCK2 decreased the proliferation, migration and invasiveness of MHCC97H and HepG2 cells. Overall, these observation suggest that miR‑130a is a regulator of ROCK2 and can inhibit proliferation, migration and invasive ability of HCC cells, at least in part, by suppressing the expression of ROCK2. The current study provides further insight into the molecular mechanisms of HCC pathogenesis and suggests a new potential biotarget for HCC treatment.