miR-23a enhances cytoxicity of etoposide in human HCC. A shows etoposide exhibits more toxic to HCC cells with ectopic miR-23a expression. HepG2 and MHCC97L cells with or without expressing ectopic miR-23a were treated with etoposide for 24 and 48 h. Cytotoxicity was evaluated with MTT assay. Increasing cell death after etoposide treatment was observed in miR-23a-overexpressed HCC cells; B shows ectopic miR-23a could significantly potentiate HCC cells to doxorubicin treatment. HepG2 and MHCC97L cells with or without expressing ectopic miR-23a were treated with doxorubicin for 24 and 48 h. Cytotoxicity was evaluated with MTT assay. C shows that miR-23a overexpression enhances inhibition of HCC tumorigenesis by etoposide. Mice were subcutaneously injected with MHCC97L cells with or without ectopic miR-23a and treated with etoposide (25 mg/kg/2 days, i.p.). Megascopic xenograft was recorded. Delayed presence of megascopic tumor was observed in miR-23a-expressed group. D shows that miR-23 overexpression increase tumor response to etoposide. After treatment for 3 weeks, tumor was dissected out and calculated. Significant reduction on tumor size could be found in miR-23a-expressed group. This picture presents the 3 representatives in each group.