Fig. 5
From: A truncating mutation in the autophagy gene UVRAG drives inflammation and tumorigenesis in mice
UVRAGFS predisposes mice to colitis-associated colon cancer. a Representative macroscopic images of the colon from AOM-DSS-treated control (Ctrl) and iUVRAGFS mice in the presence/absence of Dox at the time of necropsy (day 60). Red arrows highlight colonic tumors. b–d The number (b), size (c), and overall load (d) of colonic tumors in AOM-DSS-treated mice in a. Tumor load is evaluated by totaling the diameters of all tumors in AOM-DSS-treated mice in a. n = 5–12 mice per genotype. e IHC staining of Ki67, cleaved caspase 3, p62, keratin 20, E-cadherin, N-cadherin, and vimentin in the colons from AOM-DSS-treated mice of indicated genotypes. Data are from one animal that is representative of 5–12 animals in each group. The levels of Ki67 staining (top right) and tumor apoptosis (bottom right) in the indicated colon were quantified. Arrows (red) denote cells undergoing apoptosis. Scale bars, 100 μm. f H&E-stained sections of the colon from AOM-DSS-treated mice in a. Data are from one animal that is representative of 5–12 animals in each group. Scale bars, 100 μm. g Histological scores for crypt damage (top) and total histological score (bottom) of colons from mice in a were quantified at day 60 as described in the Methods. n = 10 mice per group. h WB analysis of caspase-1 cleavage, IL-1β production, LC3-I/II, and p62 levels in colon tissues of Dox-treated control and iUVRAGFS mice after AOM-DSS treatment. Data in h are from one experiment that is representative of three independent experiments. For all quantifications, data (mean ± SD) were from the indicated number of independent experiments and analyzed with one-way ANOVA. n.s., not significant; *P < 0.05; ***P < 0.001; ****P < 0.0001. Source data are provided as a Source Data file. See Supplementary Fig. 9 for uncropped data of h.
