Fig. 4

p-P53-Noxa was responsible for EOAI-induced apoptosis in NSCLC cells. Noxa was critical for apoptosis induced by EOAI in NSCLC cells. After being transfected with the control siRNA or Noxa siRNA, A549 and H460 cells were treated with EOAI (2 μΜ) for 48 h. A Apoptosis was quantified by Annexin V-FITC/PI double-staining analysis (left panel), and Annexin V + cell populations were defined as apoptosis (right panel). B The efficiency of siNoxa and its effect on the level of cleaved PARP. A549 and H460 cells were treated as described in panel A, and cell proteins were extracted for Western blotting analysis. GAPDH was used as the loading control. C The screen of Noxa-related transcription factors. A549 and H460 cells were treated with DMSO or EOAI, and cell lysates were measured by Western blotting with specific antibodies. GAPDH was used as the loading control. D The expression of P53 was responsible for EOAI- induced apoptosis in NSCLC cells. After transfected with the inhibitor of P53, Pifithrin-β (PFT), A549, and H460 cells were further treated with EOAI (2 μΜ) for 48 h. Apoptosis was examined by Annexin V-FITC/PI double-staining analysis (left panel), and Annexin V + cell populations were defined as apoptosis (right panel). E The knockdown efficiency of PFT and its effect on the expression of Noxa and cleaved PARP were measured by Western blotting analysis. GAPDH was used as the loading control