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. Author manuscript; available in PMC: 2024 Apr 1.
Published in final edited form as: Gastroenterology. 2023 Jan 10;164(4):593–609.e13. doi: 10.1053/j.gastro.2023.01.002

Figure 3.

Figure 3.

Tuft cells show stemness to give rise to colonic tumors in DSS-induced colitis. (A) Experimental setup to assess the ability of DSS, TNBS, oxazolone (Oxa), C rodentium (Citro), F nucleatum, and doxorubicin (Doxo) to induce tumorigenesis in Dclk1CreERT2;R26tdTomato;APCfl/fl mice treated with 3 injections of 6 mg/kg tamoxifen (TAM). (B–D) Gross pathology of the colon (B), average colonic tumor number per mouse (C), and percentage of mice (D) with colonic tumors in tamoxifen-treated in Dclk1CreERT2;R26tdTomato;APCfl/fl mice treated with vehicle or various colitis-inducing agents (n ≥ 6 per group). (E) Representative images of the colonic crypts from Dclk1CreERT2;R26tdTomato;APCfl/fl mice. DAPI, 4′,6-diamidino-2-phenylindole. DSS induces Dclk1 lineage-labeled tumors, whereas Dclk1+ cells remaining as single cells in mice treated with TNBS, oxazolone, C rodentium, and doxorubicin. Scale bar: 50 μm. (F–G) Representative immunofluorescence staining (F) and quantification (G) of Dclk1 in colonic tissues of C57BL/6J wild-type mice reveal reduced Dclk1+ cell number in DSS- and oxazolone-treated mice and increased Dclk1+ cell number in C rodentium–inoculated mice. Scale bar: 100 μm. Data in all bar graphs are presented as mean ± SEM. Asterisks above each bar indicate significant differences from the control group. *P < .05, **P < .01, ***P < .001, ****P < .0001.