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. 2015 Mar 27;15:189. doi: 10.1186/s12885-015-1230-0

Figure 1.

Figure 1

NPC1L1 knockout protects mice against colitis-associated tumorigenesis.(A) NPC1L1 protein expression was absent in the small intestine 2/5 of NPC1L1−/− mice by western blot analysis. (B) Colorectal tumorigenesis was induced by injection of the procarcinogen AOM followed by one round of DSS exposure to elicit colitis. WT mice and NPC1L1−/− mice were sacrificed at 10 weeks (10 W), 15 weeks (15 W), 18 weeks (15 W) or 20 weeks (20 W) after AOM injection, respectively. (C-F) Tumors were measured and divided into four groups according to the maximum diameter (Group 1: ≤4 mm; Group 2: >4 mm but ≤7 mm; Group 3: >7 mm but ≤10 mm; Group 4: >10 mm). Tumor number of each group and total tumor number distribution was diagrammed. With increased time post-injection, tumors increased in numbers and size. NPC1L1−/− mice had fewer tumors than WT mice. **p < 0.01, #p = 0.095 compared to WT. (G) When mice were sacrificed, colorectums (The cecum was not included.) were measured. There was not any significant difference in colon length between NPC1L1−/− mice and WT mice at any time points.