Fig. 6: RAI16 deficiency promotes colitis-associated dysplasia progression.

a Schematic representation of the AOM-DSS treatment. b Kaplan–Meier survival curve of WT (n = 15) and RAI16^−/− (n = 20) mice throughout the AOM-DSS regimen based on severe body weight loss as a consequence of excessive intestinal inflammation. P value was determined with Log-rank Mantel–Cox test. c Body weight loss of WT and RAI16^−/− mice treated as in b. d Photographs of gross representative appearance of the colons of WT and RAI16^−/− mice on day 95 post-treatment with AOM-DSS. e The average tumor numbers of WT and RAI16^−/− mice. f The average tumor sizes of in WT and RAI16^−/− mice. g, h Hematoxylin and eosin (H&E) staining of colon tissue section from WT and RAI16^−/− mice treated with AOM-DSS. Pathology scores evaluating colon tissue inflammation and ulceration of WT and RAI16^−/− mice were shown on the right panels g. Much more low-grade dysplasia was found in RAI16^−/− colon. The percentage of low-grade dysplasia was shown on the right panels h. i Colon sections were immunostained with anti-Ki67 antibody and Ki-67-positive cells were enumerated. Data represent mean ± SD of at least three independent experiments. *p < 0.05, **p < 0.01.