Fig. 7

Activation of p53 enables EOAI-induced cell cycle arrest, apoptosis, and autophagy. A Inactivation of p53 reduced the extent of G2/M cell cycle arrest. A549 and H460 cells were treated with EOAI single (2 μM) or combined with PFT (10 mM). The cell cycle profile was analyzed by PI staining and FACS, and Modfit and GraphPad Prism8 software analyzed cell distribution. B PFT reduced EOAI-induced autophagy. A549 and H460 cells were treated with EOAI single (2 μM) or combined with PFT (10 mM). LC3 was detected using immunofluorescence assay, representative pictures were captured (left panel), and LC3 puncta cells were statistically analyzed (right panel). Statistical significances of differences between groups in right panels of A and B were assessed by the t-test of GraphPad Prism8 software. * Represents a significant difference between the two groups (P < 0.05). All data were representative of at least three independent experiments (n = 3; error bar, SD). C Effect of PFT on protein expression of p21, p27, p-AMPKα, and LC3. A549 and H460 cells were treated with EOAI single (2 μM) or combined with PFT (10 mM). Cell proteins were detected using specific antibodies. GAPDH was used as the loading control. All data were representative of at least three independent experiments. D Schema of the mechanism for EOAI-induced cell cycle arrest, apoptosis, and autophagy in NSCLC. EOAI treatment-induced DNA damage and led to G2/M cell cycle arrest by p53-p21/p27 axis; triggered apoptosis through regulating pro-apoptotic proteins including Bax and Noxa; and stimulated autophagy through p53-dependent AMPK activation