Figure 2.
Inflammasome in tumor suppression. (A) Hematoxylin and eosin (H&E) staining of colon sections derived from WT, Casp1-/- , Asc-/- and Casp12 -/- mice on days 0 and 8 after the start of DSS treatment (magnification 100×). (B, C), Immunofluorescence was performed on colon sections derived from WT, Casp1-/- , Asc-/- and Casp12 -/- mice on days 0 and 8 for examination of proliferating cells (PCNA) (B) and tight junction (Claudin-3) (C); (magnification 100×). , WT and Nlrp6–/– (D), Nlrp12–/– (E), Nlrp3–/– (F), and Nlrc4–/– (G–I) mice were injected s.c. with 1 × 105 B16F10 cells. (D-F, H) Tumor mass was determined at 16 to 20 days after inoculation. (G) WT and Nlrc4–/– tumor areas (length × width) were measured every 2 to 3 days. (I) Representative images of excised WT and Nlrc4–/– B16F10 tumors. (G, H) Data are representative of 3 independent experiments with n = 5 mice per group. (J, K) Mini-endoscopy (J) and representative images (K) of colons from AOM/DSS-treated wild-type (n = 5), Asc−/− (n = 3) and Aim2−/− mice (n = 5). (L) Macroscopic polyp counts, average polyp size per mouse and tumor load (n = 21 for WT, n = 18 for Aim2−/− and n = 10 for Asc−/− ). (M, N) Semiquantitative scoring of colon hyperplasia (M) and dysplasia (N) in AOM/DSS-treated wild-type and Aim2−/− mice (n = 6 for WT AOM/mock and Aim2−/− AOM/DSS, and n = 5 for WT AOM/DSS and Aim2−/− AOM/mock). The figures A–C are reprinted with permission from Ref (39). Copyright Cell Press. The figures D–I are reprinted with permission from Ref (44). Copyright American Society for Clinical. The figures (J–N) are reprinted with permission from Ref (43). Copyright Nature Publishing Company. *P<0.05, **P<0.01, ***P<0.001, ns: no significance.