Figure 4

JNK is involved in transmitting the signal from Hh to Gli in acquired chemoresistant cancer cells. Values of the blots (p-JNK) relative to GAPDH quantified by Image J are statistical different (data not shown). A-B, Treatment with Hh inhibitors Robo (A) and cyc (B) suppresses the phosphorylation of JNK in acquired chemoresistant cancer cells. Blots are representative data from at least three independent experiments. C, Exposure of NIH-3 T3 cells to SHh causes phosphorylation of JNK. 293 T cells were treated with SHh (100 ng/ml) for different times as indicated, and were harvested for western blot analysis. GAPDH were used as a loading control. Blots are representative results from at least three separate experiments. D, K562/A02 cells and its parental K562 cells were transfected with Gli luciferase reporter and pRL-Renilla luciferase plasmids, and were treated with peptide JNK inhibitor JIP for 24 h. Data are mean ± s.d. from three separate experiments. E, Acquired chemoresistant cancer cells K562/A02, KB/VCR and their respective parental cells K562 and KB were transfected with Gli luciferase reporter and pRL-Renilla luciferase plasmids with GFP or Gαt. Data are mean ± s.d. from three separate experiments. F, KV/VCR cells were transfected with Gli luciferase reporter and pRL-Renilla luciferase plasmids, and were treated with SAG with or without JIP for 36 h. Data are mean ± s.d. from three separate experiments.