Liquiritigenin inhibits colorectal cancer proliferation, invasion and epithelial to mesenchymal transition by decreasing expression of runt-related transcription factor 2.

Inhibition of tumor metastasis is one of the most important purposes in colorectal cancer (CRC) treatment. This study aimed to explore the effects of liquiritigenin, one of flavonoids extracted from the roots of Glycyrrhiza uralensis Fisch, on HCT116 cell proliferation, invasion, and epithelial to mesenchymal transition (EMT). We found that liquiritigenin significantly inhibited HCT116 cell proliferation, invasion and EMT process but had no influence on cell apoptosis. Moreover, liquiritigenin remarkably reduced the expression of runt-related transcription factor 2 (Runx2) in HCT116 cells. Overexpression of Runx2 obviously reversed the liquiritigenin-induced invasion and EMT inhibition. Furthermore, liquiritigenin inactivated the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway in HCT116 cells. Up-regulation of Runx2 reversed the liquiritigenin-induced PI3K/AKT pathway inactivation. In conclusion, our research verified that liquiritigenin exerted significant inhibitory effects on CRC invasion and EMT process by down-regulating the expression of Runx2 and inactivating PI3K/AKT signaling pathway. Liquiritigenin could be as an effective therapeutic and prevention medicine for CRC treatment.