Fig. 4.

Molecular pathway analysis of cell signalling inhibition by D1 peptide. a KM12SM and SW620 colorectal cancer cell lines or b U87 and U118 glioblastoma cells were treated with IL-13 for the indicated times in serum-free DMEM in absence or presence of D1 peptide. Cell extracts were analysed by western blot with antibodies against FAK, JNK, ERK1/2, Src, AKT and their phosphorylated forms. The D1 peptide inhibited phosphorylation of IL-13 mediators in a time and cell type-dependent mode. c KM12SM and U251 cells were treated with IL13 and/or D1 peptide for 1 h and analysed by flow cytometry to detect cell surface IL13Rα2 or (d) by western blot for total IL13Rα2. Whereas IL13 significantly promoted receptor internalisation (**p < 0.01; ***p < 0.001), D1 significantly inhibited IL13-triggered internalisation (◊◊p < 0.01; ◊◊◊p < 0.001). RhoGDI was used as loading control