Isoliquiritigenin inhibits cell proliferation and migration through the PI3K/AKT signaling pathway in A549 lung cancer cells.

The present study aimed to investigate the molecular mechanisms of inhibition of Isoliquiritigenin (ISL) on the proliferation and migration of A549 cells. A549 cells were cultured in vitro, and the effects of ISL inhibition were examined using cell counting kit-8, Transwell invasion and flow cytometric assays. Western blot analysis was also performed to detect cell apoptosis and the expression of phosphatidylinositol 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) signaling pathway-associated proteins. The results demonstrated a significant inhibition of proliferation and migration of A549 cells when treated with ISL (P<0.05). Furthermore, ISL treatment significantly downregulated the expression of E-cadherin, and upregulated the expression of N-cadherin and vimentin. Flow cytometric analysis revealed a significant increase in cell apoptosis in the ISL group as well as the expression of pro-apoptotic proteins Bcl-2-associated X protein and active caspase-3. Conversely, the expression of anti-apoptotic protein B-cell lymphoma 2 was decreased. There was a significant decrease in the phosphorylation of AKT and mammalian target of rapamycin, and in the expression of cell proliferation proteins P70 and cyclin D1 in ISL-treated cells. In conclusion, ISL has significant inhibitory effects on the proliferation and migration of A549 cells by promoting cell apoptosis. The mechanism may involve of PI3K/AKT signaling pathways in A549 cells, which may a potential therapeutic target for the treatment of lung cancer.