BAICALEIN INHIBITS EMT OF LUNG CANCER CELLS AND ENHANCES THE CYTOTOXICITY OF CISPLATIN BY REGULATING THE PI3K/AKT/NF-KB SIGNALING PATHWAY

Objective: To explore the mechanism of baicalein inhibiting the epithelial to mesenchymal transition (EMT) of lung cancer cells and enhancing the cytotoxicity of cisplatin by regulating the PI3K/Akt/NF-kappa B signalling pathway. Methods: A549/CDDP cells were treated with LY294002 and baicalin at different concentrations (0 mu m, 12.5 mu m, 25 mu m, 50 mu m, 100 mu m). The effects of LY294002 and baicalin on the invasion and migration ability of A549/CDDP cells were observed. In the Control Group: A549/CDDP cells were observed without any treatment. In the Negative Control: the expression of p65 in A549/CDDP cells and the p65 siRNA group were silenced to observe the effect of siRNA on the expression of p65 after A549/CDDP transfer. After silencing the expression of p65, the expression of vientin and the effect of interfering p65 expression on the invasion and migration of cells were observed. Results: After 48 h, the expression level of the EMT marker E-cadherin protein in the A549/CDDP cells of the baicalein group was significantly higher than that of the control group, and the expression level of the Vimentin protein was significantly lower than that of the control group, which was dose-dependent (P<0.05). The invasion and migration ability of the baicalein group was significantly weaker than that of the control group (P<0.05) after 48 h. The expression level of p-AKt in A549/CDDP cells was significantly higher than that in A549 cells (P<0.05). Moreover, after LY294002 was added, the expression level of p-AKt was significantly lower than that of the control group (P<0.05). The expression level of E-cadherin in the LY294002 group was significantly higher than that of the control group (P<0.05), and the expression level of Vimentin was significantly lower than that of the control group (P<0.05). The invasion and migration ability of LY294002 group was significantly stronger than that of the control group (P<0.05). The expression of p-AKt and Akt in the baicalein group was significantly lower than that in the control group, and the expression was dose-dependent (P<0.05). The expression level of E-cadherin in the p65 siRNA group was significantly higher than that of the control group, and the expression level of Vimentin was significantly lower (P<0.05). The invasion and migration ability of the p65 siRNA group was significantly weaker than that of the control group (P<0.05). The expression level of p65 in the baicalein group was significantly lower than that in the control group; the expression level of I kappa B alpha was significantly higher than that in the control group, and it was dose-dependent (P<0.05). In group LY294002, the expression of I kappa B alpha was significantly stronger than that of the control group, and the expression of p65 was significantly lower than that of the control group (P<0.05). Conclusion: The enhancement of lung cancer cytotoxicity by baicalein may be achieved by blocking the PI3K/Akt/NF-kappa B signalling pathway to inhibit EMT and then inhibiting the expression of anti-apoptotic genes.