Fig. 2: Uhrf1ki/ki mice are resistant to AOM/DSS-induced colorectal tumorigenesis.

A Experimental scheme for induction of colorectal tumors in Uhrf1+/+ and Uhrf1ki/ki mice by AOM/DSS treatment. B Representative macroscopic images of AOM/DSS-induced colorectal tumors from Uhrf1+/+ and Uhrf1ki/ki mice. Comparison of total number of tumors per mouse (C) and sizes of tumors (D) from AOM/DSS-treated Uhrf1+/+ and Uhrf1ki/ki mice. The tumor size was measured by stereomicroscope. Error bars, S.E. Uhrf1+/+, n = 19; Uhrf1ki/ki, n = 8. **p < 0.01; *p < 0.05. E Tumors were classified according to the size ranges (L > 3 mm; 3 > L > 2 mm, and L < 2 mm) and plotted as number of tumors per mouse. L: diameter of tumor. Error bars, S.E. Uhrf1+/+ (n = 19); Uhrf1ki/ki (n = 8). **p < 0.01; *p < 0.05. F Representative H&E staining images of colon cross-sections. Tumor lesions in Uhrf1+/+ mice and Uhrf1ki/ki mice are marked in blue or red circle, respectively. Upper scale bars, 2 mm. Bottom scale bars, 50 μm. G DNA-methylation levels in colon tissues from control Uhrf1+/+ and Uhrf1ki/ki mice or tumors from AOM/DSS-treated Uhrf1+/+ and Uhrf1ki/ki mice. For control group, Uhrf1+/+, n = 3; Uhrf1ki/ki, n = 3. For AOM/DSS-treated mice, Uhrf1+/+, n = 6; Uhrf1ki/ki, n = 6. Genomic DNA was prepared from normal epithelium cells or microdissected tumor tissues, and 5mC level was measured by HPLC. Error bars, S.E.