Fig. 6: Activation of IRF3 by PRR signaling relieves its inhibition on Wnt signaling.
From: IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin
a TOPflash-relative luciferase activity analysis for VSV treatment in IRF3-knockout HCT116 cells. b Nucleocytoplasmic separation and immunoblot analysis of active-β-catenin (active-β-cat.) and IRF3 activation in HCT116 cas9 cells after treated with VSV. c TOPflash-relative luciferase activity analysis for VSV treatment in siNC and siIRF3 HCT116 cells. d Immunoblot analysis for the interaction between IRF3, IRF3-ΔnDB, IRF3-ΔNLS, or IRF3-5D and β-catenin with anti-FLAG immunoprecipitates of HEK293T cells. e Immunoblot analysis for the interaction between IRF3 or IRF3-5D and β-catenin-S33A with anti-FLAG immunoprecipitates in HEK293T cells. f Immunoblot analysis for the endogenous interaction between active-β-catenin or β-catenin and IRF3 with anti-IRF3 immunoprecipitates in HCT116 cell line extracts treated with VSV. g Representative images of the small intestine tumors from 5-month-old Apcmin/+ and Apcmin/+ IRF3−/− mice with 4 months Abx treatment. h The small intestine tumor counts from Apcmin/+ and Apcmin/+ IRF3−/− mice with Abx treatment (n = 10, n = 11, n = 10, n = 10). i Standardized TCF1 and MX1 immunostaining of the small intestine and tumors from Apcmin/+ and Apcmin/+ IRF3−/− mice with Abx treatment or without Abx treatment. Scale bars, 50 μm. Each symbol represents one mouse (h). *P < 0.05; **P < 0.01; ***P < 0.001; NS not statistically significant by two-tailed t test (a, c, h). Data are from two (g–i) or three (a–f) independent experiments and are presented as mean ± s.e.m. in a, c, h. Source data are provided as a Source data file. See also Supplementary Fig. S6.
