Figure 3
HER2 is overexpressed and both Herceptin incubation and siRNAs against HER2 reversed the EMT in cisplatin-resistant gastric cancer cells.
(A) Western blot of HER2 in MGC803/DDP and AGS/DDP cell lines and parental MGC803 and AGS cells. GAPDH was used as loading control. (B) Relative amplification of HER2 in parental and cisplatin-resistant cells. Results were presented as the mean ± SD of two independent experiments, *P < 0.05 compared with parental cells. (C) Herceptin incubation abrogated EMT morphology in MGC803/DDP cells. Representative images of cellular morphology of MGC803/DDP cells, plus parental MGC803 cells treated with Herceptin for 24 h were shown. Hercep represents Herceptin. (D) Herceptin incubation reversed EMT morphology in MGC803/DDP cells. Representative images of FITC-phalloidin staining of F-actin after 100 μg/ml Herceptin treatment for 24 h were shown. (E) Effects of Herceptin on levels of ZO1 and Snail. (F) CP724714 treatment abolished EMT-like cell morphology. Cells were incubated with 10 μM CP724714 for 24 h. Representative images of cellular morphology of were captured. (G) CP724714 treatment abrogated EMT-like cell morphology. Cells were treated as in Fig. 4F, FITC-phalloidin staining of F-actin was performed and typical images were shown. (H) Effects of CP724714 on ZO1 and Snail. (I) CP724714 inhibited the increased cell migration in cisplatin-resistant gastric cancer cells. Representative images were presented here. (J) CP724714 inhibited the increased cell migration in cisplatin-resistant gastric cancer cells. Values represented the mean ± SD from three independent experiments with triplicate samples. *P < 0.01.
