The expression status and potential mechanistic involvement of microRNA (miR)-126-5p in hepatocellular carcinoma (HCC) are still elusive currently. Here we set out to address this issue both in cell lines and in patients’ tissues.

The relative expression levels of endogenous miR-126-5p and epidermal growth factor receptor (EGFR) were quantified by real-time polymerase chain reaction. Cell viability and proliferation were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and clonogenic assays, respectively. Cell invasive and migrative capacities were determined by transwell and wound healing assays, respectively. The regulatory action of miR-126-5p on EGFR was interrogated by luciferase reporter assay. Translational level of EGFR was analyzed by Western blotting.

MiR-126-5p was significantly down-regulated in both HCC patients’ tissues and cell lines. Forced expression of miR-126-5p greatly compromised cell viability, proliferation, invasion and migration, while miR-126-5p-specific inhibitor promoted these oncogenic phenotypes. MiR-126-5p mimics inhibited endogenous expression of EGFR and suppressed EGFR 3′-untranslated region-fused luciferase activity. Co-expression of EGFR in miR-126-5p-proficient cells completely restored cell migrative and invasive capacities, while co-transfection with EGFR siRNA significantly inhibited miR-126-5p inhibitor-induced cell invasion and migration.

MiR-126-5p was aberrantly decreased in HCC and subsequently relieved the suppression on EGFR expression, which consequently contributed to the tumor biology of HCC.