Autophagy inhibition enhances apigenin-induced apoptosis in human breast cancer cells

摘要: Apigenin (4',5,7-trihydroxyflavone) is a member of the flavone subclass flavonoids present in fruits and vegetables. The involvement autophagy apigenin-induced apoptotic death human breast cancer cells was investigated. Cell proliferation viability were assessed by 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) clonogenic assays. Flow cytometry, fluorescent staining Western blot analysis employed to detect apoptosis autophagy, role using inhibitors. dose- time-dependently repressed survival T47D MDA-MB-231 cell lines. due associated with increased levels Caspase3, PARP cleavage Bax/Bcl-2 ratios. results from flow cytometry also verified occurrence apoptosis. In addition, apigenin-treated exhibited as characterized appearance autophagosomes under fluorescence microscopy accumulation acidic vesicular organelles (AVOs) cytometry. Furthermore, revealed that level LC3-II, processed form LC3-I, increased. Treatment inhibitor, 3-methyladenine (3-MA), significantly enhanced induced apigenin, which accompanied an increase cleavage. Similar confirmed microscopy. These indicate apigenin has apoptosis- autophagy-inducing effects cells. Autophagy plays cyto-protective apoptosis, combination inhibitor may be promising strategy for control.