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

Ono, Junya; Shime, Hiroaki; Takaki, Hiromi; Takashima, Ken; Funami, Kenji; Yoshida, Sumito; Takeda, Yohei; Matsumoto, Misako; Kasahara, Masanori; Seya, Tsukasa

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

Ono, Junya; Shime, Hiroaki; Takaki, Hiromi et al.

Journal of biomedical science, 2017, 24, 79

Permalink : https://hdl.handle.net/2115/67976

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/67976
タイトル	The TLR3/TICAM-1 signal constitutively controls spontaneous polyposis through suppression of c-Myc in ApcMin/+ mice
著者	Ono, Junya ; Shime, Hiroaki ; Takaki, Hiromi ; Takashima, Ken ; Funami, Kenji ; Yoshida, Sumito ; Takeda, Yohei ; Matsumoto, Misako ; Kasahara, Masanori ; Seya, Tsukasa
著者名 Ono, Junya
e-Rad_Researcher 70372133 著者名 Shime, Hiroaki
著者名 Takaki, Hiromi
著者名 Takashima, Ken
e-Rad_Researcher 00421983 著者名 Funami, Kenji
著者名 Yoshida, Sumito
著者名 Takeda, Yohei
e-Rad_Researcher 30332456 著者名 Matsumoto, Misako
e-Rad_Researcher 30241318 著者名 Kasahara, Masanori
e-Rad_Researcher 10301805 著者名 Seya, Tsukasa
言語	英語
キーワード	TLR3
	TICAM-1 (TRIF)
	c-Myc
	Intestinal polyposis
発行日	2017-10-17
出版者	BioMed Central
収録物名	Journal of biomedical science
巻(号)	24
ページ	79
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
権利情報	Creative Commons Attribution 4.0 International
PISSN	1021-7770
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1186/s12929-017-0387-z