Effects of glabridin on malignant biological behaviors of lung adenocarcinoma A549 cells and its molecular mechanism
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Abstract:
Objective: To study the effects of glabridin on malignant biological behaviors of lung adenocarcinoma A549 cells and its molecular mechanism. Methods: A549 cells and human normal lung epithelial BEAS-2B cells were cultured by conventional methods and then treated with different concentrations of glabridin and/or cisplatin. The effects of glabridin and cisplatin on the proliferative vitality of A549 and BEAS-2B cells were detected by crystal violet staining and CCK-8 method. Transwell cell assay and cell scratch assay were used to detect the effect of glabridin on the invasion and migration ability of A549 cells. Flow cytometry was conducted to detect the effect of glabridin on the apoptosis of A549 cells. 3D ultra-low adhesion plate culture method was applied to culture A549cells, and then the effects of glabridin on the proliferation of A549 cells and the expression of epithelial mesenchymal transition (EMT)-related proteins in A549 cells were detected using CCK-8 method and Western-blot, respectively. An A549 cell-transplanted tumor model was constructed to detect the effects of glabridin and cisplatin on the growth of transplanted tumors and the expression of EMT-related proteins in transplanted tumor tissues. Results: Glabridin and cisplatin significantly inhibited the proliferation (P<0.05 or P<0.01), cell migration (P<0.05 or P<0.01) and invasion (P<0.05 or P<0.01) of A549 cells in a dose-dependent manner. Glabridin could induce the apoptosis of A549 cells (P<0.01), inhibit the protein expression of N-cadherin, snail, and vimentin, but promote the protein expression of E-cadherin in A549 cells. Both glabridin and cisplatin could inhibit the growth of A549 cell-transplanted tumors,inhibit the protein expression of Ki67, N-cadherin, snail, and vimentin, and promote the protein expression of E-cadherin in transplanted tumor tissues. Conclusion: Glabridin can inhibit the proliferation, migration, and invasion of A549 cells, induce apoptosis of A549 cells, and inhibit EMT processes, thus exerting anti-tumor effect.