Fig. 3
From: Evasion of immunosurveillance by genomic alterations of PPARγ/RXRα in bladder cancer
RXRαS427F/Y functionally promotes ligand-independent PPARγ signaling in human bladder cancer lines. a Heat map representing pathways activated/suppressed in RXRαS427Y, RXRαS427F and PPARγ overexpressing lines relative to their respective controls. Orange represents pathway activation and blue represents pathway suppression. The analysis was based on three biological replicates. b Upper, western blot of RXRα confirming overexpression of RXRαWT (WT), RXRαS427F (S427F) and RXRαS427Y (S427Y) in T24 cells relative to control (Vec). Lower, RT-qPCR analysis of ANGPTL4 and PLIN2 in various engineered lines. c Upper, western blot confirming overexpression of PPARγ in T24 line relative to control (Vec). Lower, RT-qPCR analysis of ANGPTL4, PLIN2, ACOX1 and PDK4 in engineered lines. d Upper, western blot of RXRα and PPARγ in SV-HUC line engineered to inducibly overexpress RXRαS427F and knockdown PPARγ by multiple shRNAs (sh#4, 5 and 9) upon doxycycline (DOX) treatment. Lower, RT-qPCR analysis of PLIN2, ACOX1 and PSCA in various SV-HUC-1 engineered lines. +/− represents presence or absence of DOX treatment respectively. e RT-qPCR analysis of ANGPTL4 and PLIN2 in HT-1197 (carrying endogenous RXRAS427F), 5637 and UM-UC9 (PPARG amplified) lines treated with DMSO or T0070907 for 24 h. All RT-qPCR data is normalized to GAPDH and presented as mean fold change vs. control ± SEM of at least three biological replicates
