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. 2020 Jun 1;10(4):729–746. doi: 10.1016/j.jcmgh.2020.05.010

Figure 1.

Figure 1

Intestinal epithelial cell VDR KO mice developed more tumors. (A) Schematic overview of the AOM/DSS-induced colon cancer model. AOM (10 mg/kg) was injected on day 0. On day 7, 2% DSS solution was administered to mice in drinking water. Seven days of DSS was followed by 3 weeks of drinking water. An additional 2 cycles of DSS were administered before killing. At week 15, mice were killed. (B) Colonic tumors in situ. Representative colons from different groups. Tumors are indicated by red arrows. (C) Tumor numbers in AOM/DSS-induced colon cancer model: VDRLoxP and VDRΔIEC mice. Data are expressed as means ± SD. n = 25–30, 1-way analysis of variance test. No tumors in controls for VDRLoxP and VDRΔIEC mice, therefore controls are not included for comparisons. (D) Maximum tumor size in the AOM/DSS-induced colon cancer model: VDRLoxP and VDRΔIEC mice. Data are expressed as means ± SD. n = 25–30, 1-way analysis of variance test. (E) The distance of each tumor to the anus was measured. Data are expressed as means ± SD. n = 25–30, 1-way analysis of variance test. (F) Representative H&E staining of Swiss rolls of representative colons from the indicated groups. Images are from a single experiment and are representative of 10 mice per group. (G) Quantitation of PCNA-positive cells in control mucosa/per intestinal glands or in the tumor tissue/high-power field. PCNA expression in the tumor tissue of VDRΔIEC mice was significantly higher than that in the VDRLoxP mice. Data are from a single experiment and are representative of 5 mice per group. Data are expressed as means ± SD. n = 5, Student t test. ∗P < .05.