Accumulation of proteins associated with the ER stress pathway for apoptosis in response to homoisoflavanone-1 treatment. A549 cells were treated with homoisoflavanone-1 (100 µg/ml) for 0, 6, 12 and 24 h. (A) Western blot analysis was performed to detect the protein expression of (B) PERK, ATF4 and GADD34. A549 cells were treated with 0, 12.5, 25, 50 or 100 µg/ml of homoisoflavanone-1 for 12 h and (C) western blot analysis was performed to detect the protein expression of (D) PERK. A549 cells were treated with 0, 12.5, 25, 50 or 100 µg/ml of homoisoflavanone-1 for 24 h and (E) western blot analysis was performed to detect the protein expression of (F) ATF4 and (G) GADD34. β-actin was the loading control. Data are presented as the mean ± standard deviation from three independent experiments. *P<0.05 and **P<0.01 vs. the control group. ER, endoplasmic reticulum.