Effects of Baicalin on Cell Autophagy and Epithelial-Mesenchymal Transformation in Lung Cancer A549 Cells

This work was to investigate the effects of baicalin on cell autophagy, EMT (epithelialmesenchymal transition) and cell invasion in lung cancer A549 cells. The effect of Baicalin (0, 5, 10, 20, 40, 80, 160, 320, 640 μmol/L) on the viability of A549 cells was measured by MTT assay. Formation of autophagosome was observed by staining with acridine orange under fluorescence microscope. The morphological changes of A549 cells were observed under microscope. The cell invasion ability was analyzed by Transwell method. The protein expression of E-cadherin, Vimentin and LC3 in A549 cells was detected by Western blot. The activity of A549 cells was significantly inhibited by Baicalin in a dose dependent manner (P<0.05). IC50 of Baicalin (24 h) for A549 cells was 104.30 μmol/L. Acridine orange fluorescent staining showed that the number of intracellular acid dye follicular bright red fluorescence in the A549 cells was significantly increased after Baicalin treatment, while the autophagic lysosomes were rarely observed in control group. The protein level of LC3-II/GAPDH in A549 cells was significantly enhanced after Baicalin treatment (P<0.01). TGF-β1 could induce morphological alteration of the A549 cells from epithelial morphology to mesenchymal morphology. Meanwhile, the protein expression of E-cadherin was down-regulated and the protein expression of Vimentin was up-regulated in the presence of TGF-β1 (5 ng/mL) (P<0.01). Baicalin significantly inhibited TGF-β1induced cell invasion. Moreover, Baicalin reversed TGF-β1-induced EMT, up-regulating the protein expression of E-cadherin and down-regulating the protein expression of Vimentin (P<0.01). In conclusion, Baicalin significantly inhibits the growth and induces autophagy in A549 cells, meanwhile reversing TGF-β1-induced EMT in lung cancer A549 cells.