Emodin has anti-inflammatory, antioxidant and antitumor effects. This study discusses the effect and molecular mechanism of emodin on hepatocellular carcinoma cells by medical experimental methods and bioinformatics analysis.

Huh7 cells were treated with different concentrations, then real-time fluorescence quantitative polymerase chain reaction (qPCR) and Western blotting were used to determine the expression of miR-429 and SOX2. SOX2 overexpression plasmid, miR-429 inhibitor and miR-429 mimics were synthesized and then transfected into Huh7 cells, and the expression changes of miR-429 and SOX2 were verified by qPCR and Western blotting, the functional changes of cells were observed by CCK-8 and transwell assay. Finally, according to the predicted binding site of TargetScan, the binding between miR-429 and SOX2 was confirmed by double luciferase reporter gene detection.

Compared with the control group, emodin at different concentrations (1, 10, 100 μmol/L) significantly promoted the expression of miR-429 and inhibited the expression of SOX2 (P<0.05). Overexpression SOX2 plasmid and miR-429 inhibitor promoted the expression of SOX2 and the ability of proliferation, migration and invasion in Huh7 cells (P<0.05). Furthermore, miR-429 mimics decreased the expression of SOX2 (P<0.05) and the ability of cell migration and invasion. In addition, miR-429 was directly banded with SOX2.

Emodin regulates miR-429/SOX2 axis to inhibit the ability of proliferation, migration and invasion in liver cells.