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

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/67976

Title: The TLR3/TICAM-1 signal constitutively controls spontaneous polyposis through suppression of c-Myc in ApcMin/+ mice
Authors: Ono, Junya Browse this author
Shime, Hiroaki Browse this author →KAKEN DB
Takaki, Hiromi Browse this author
Takashima, Ken Browse this author
Funami, Kenji Browse this author →KAKEN DB
Yoshida, Sumito Browse this author
Takeda, Yohei Browse this author
Matsumoto, Misako Browse this author →KAKEN DB
Kasahara, Masanori Browse this author →KAKEN DB
Seya, Tsukasa Browse this author →KAKEN DB
Keywords: TLR3
TICAM-1 (TRIF)
c-Myc
Intestinal polyposis
Issue Date: 17-Oct-2017
Publisher: BioMed Central
Journal Title: Journal of biomedical science
Volume: 24
Start Page: 79
Publisher DOI: 10.1186/s12929-017-0387-z
Abstract: Background: Intestinal tumorigenesis is promoted by myeloid differentiation primary response gene 88 (MyD88) activation in response to the components of microbiota in ApcMin/+ 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 ApcMin/+Ticam1-/- mice and their survival was compared to survival of ApcMin/+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 ApcMin/+ mice. TICAM-1 knockout resulted in shorter survival of mice compared to WT mice or mice with knockout of MyD88 in the ApcMin/+ background. Polyps were more frequently formed in the distal intestine of ApcMin/+Ticam1-/- mice than in ApcMin/+ 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 ApcMin/+Ticam1-/- mice compared to ApcMin/+ mice. Gene expression of inducible nitric oxide synthase (iNOS), interferon (IFN)-γ, CXCL9 and IL-12p40 was increased in polyps of ApcMin/+Ticam1-/- mice. mRNA and protein expression of c-Myc, a critical transcription factor for inflammation-associated polyposis, were increased in polyps of ApcMin/+Ticam1-/- mice. A Lactobacillus strain producing dsRNA was detected in feces of ApcMin/+ mice. Conclusion: These results imply that the TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in ApcMin/+ mice.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/67976
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 瀬谷 司

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