Fig. 6

PPARγ activation suppresses bladder cancer through inhibiting Akt pathway. (a) Blockade of PI3K-Akt signaling pathway inhibited proliferation of bladder cancer cells. Umuc-3 cells were treated with Ly294002 (10, 20, 50 μM) and MK2206 (5, 10, 20 μM) for 96 h. Cell proliferation was determined with CCK-8 every 24 h. (b) Blockade of PI3K-Akt signaling pathway induced cell apoptosis in bladder cancer cells. Umuc-3 cells were treated with Ly294002 (20 μM) and MK2206 (10 μM) for 24 h. Data are shown as mean ± standard deviation from triplicate experiments. * signifies p < 0.05; **, p < 0.01; compared with the control group treated with DMSO (0.1%). (c) Rosiglitazone hindered the growth of subcutaneous tumors generated with Umuc-3 and 5637 cells in nude mice (n = 7). (d) IHC staining of PPARγ, PTEN, and the phosphorylation of Akt (Ser473), FoxO1 (Ser256) and Bcl2 (Ser70) in subcutaneous tumors