Molecular profiling reveals potential targets in cholangiocarcinoma

Figure 4 Validation of the identified cell cycle and Notch associated genes in the triple transgenic cholangiocarcinoma mouse model. A: The cartoon diagram of the genetically engineered mouse modeling (GEM) strategies. Triple transgenic mice bearing Albumin-Cre transgene, LSL-Kras^G12D, and floxed-p53 were conditionally activated KrasG12D and heterozygous knocked out P53 in the liver. B: The genotyping data presenting positive Cre (red triangle), KrasG12D (blue triangle), and homozygous floxed P53 genes (green triangle). C: The gross image of representative tumor (upper right, scale bar = 5 mm), and the corresponding histopathology (lower right, scale bar = 100 μm) with inset showing glandular appearance (arrow, scale bar = 20 μm). D: Histology of human bile duct (upper, scale bar = 100 μm) with inset showing biliary epithelium (arrow, scale bar = 20 μm), and cholangiocarcinoma (lower, scale bar = 100 μm) with inset showing mitotic figure (arrowhead, scale bar = 20 μm) and glandular appearance (arrow, scale bar = 20 μm). E: The protein expression levels of leading-edge genes from cell cycle and Notch associated pathways, and genes involved in autophagy, cell death and DNA damage in CCA tumor tissues from the GEM (50 wk) compared to the normal bile ducts of control mice (50 wk). GAPDH was used as the loading control.