Exposure to 17-AAG results in reduced cancer cell motility and proliferation. (A) Western blotting analysis revealing the expression profile of total and phosphorylated c-Met protein in all three bladder cancer cell lines, upon a 24-hours incubation with different concentrations of 17-AAG. (B) Scratch-wound assays conducted on RT4 (i-iv), RT112 (v-viii) and T24 (ix-xii) cells, under control conditions or in the presence of 10 μM 17-AAG. T24 highly malignant cells display strong wound-healing potential (panel xi) over a 24-hours period, compared to RT4 and RT112 (panels iii and vii, respectively) cells, under control conditions. Interestingly, 17-AAG administration induces a moderate impairment of T24 cell motility and proliferative dynamics (panel xii), thus only partly prohibiting, in contrast to RT4 and RT112, the efficient closure of the gap (scratch-wound). Cells were observed under an inverted microscope and pictures were taken at a 20 × magnification. All experiments were repeated three times.