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Background  Intestinal tumorigenesis is promoted by myeloid differentiation primary response gene 88 (MyD88) activation in response to the components of microbiota in  Apc    Min/+   mice. Microbiota also contains double-stranded RNA (dsRNA), a ligand for TLR3, which activates the toll-like receptor adaptor molecule 1 (TICAM-1, also known as TRIF) pathway.    Methods  We established  Apc    Min/+    Ticam1    −/−   mice and their survival was compared to survival of  Apc    Min/+    Myd88    −/−   and wild-type (WT) mice. The properties of polyps were investigated using immunofluorescence staining and RT-PCR analysis.    Results  We demonstrate that TICAM-1 is essential for suppression of polyp formation in  Apc    Min/+   mice. TICAM-1 knockout resulted in shorter survival of mice compared to WT mice or mice with knockout of MyD88 in the  Apc    Min/+   background. Polyps were more frequently formed in the distal intestine of  Apc    Min/+    Ticam1    −/−   mice than in  Apc    Min/+   mice. Infiltration of immune cells such as CD11b +  and CD8α +  cells into the polyps was detected histologically. CD11b and CD8α mRNAs were increased in polyps of  Apc    Min/+    Ticam1    −/−   mice compared to  Apc    Min/+   mice. Gene expression of inducible nitric oxide synthase (iNOS), interferon (IFN)-γ, CXCL9 and IL-12p40 was increased in polyps of  Apc    Min/+    Ticam1    −/−   mice. mRNA and protein expression of c-Myc, a critical transcription factor for inflammation-associated polyposis, were increased in polyps of  Apc    Min/+    Ticam1    −/−   mice. A  Lactobacillus  strain producing dsRNA was detected in feces of  Apc    Min/+   mice.    Conclusion  These results imply that the TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in  Apc    Min/+   mice.    Electronic supplementary material  The online version of this article (10.1186/s12929-017-0387-z) contains supplementary material, which is available to authorized users.

The TLR3/TICAM-1 signal constitutively controls spontaneous polyposis through suppression of c-Myc in Apc Min/+ mice