Fig. 4

CLDN7 overexpression attenuated tumor proliferation and induced tumor apoptosis in vitro and in vivo. (A) MTS assay determined cell proliferation of Caki-1 CLDN7 (a) and of A498 CLDN7 (b) comparing with control cells at indicated time. (B) a. The representative images of Caki-1 CLDN7 and Caki-1 Control cells by EDU incorporation assay. Scale bar, 100 μm (left panel). Statistical analysis of cell proliferation ability of Caki-1 CLDN7 and Caki-1 Control cells by positive percentage of EDU (right panel). b. Representative images of EDU incorporation assay in A498 cells. Scale bar, 100 μm. Statistical analysis of cell proliferation ability of A498 CLDN7 and A498 Control cells by positive percentage of EDU. (C) a. Representative images of Caki-1 CLDN7 and Caki-1 Control cells stained with APC and PI measured by flow cytometer (left panel). Statistical analysis of early cell apoptosis of Caki-1 CLDN7 and Caki-1 Control cells (right panel). b. Representative images of A498 CLDN7 and A498 Control cells stained with APC and PI measured by flow cytometer (left panel). Statistical analysis of early cell apoptosis of Caki-1 CLDN7 and Caki-1 Control cells (right panel). (D) Mice experiment. a.. Images of 20 mice and xenografts formed by Caki-1 Control and Caki-1 CLDN7 cells one month after planation. b. and c. Statistical analysis of growth curves and tumor weights of xenografts derived from Caki-1 Control and Caki-1 CLDN7 cells. Data were presented as mean ± SD from at least three independent experiments. *p < 0.05, **p < 0.01