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TLR3/TICAM-1 signaling in tumor cell RIP3-dependent necroptosis

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Title: TLR3/TICAM-1 signaling in tumor cell RIP3-dependent necroptosis
Authors: Seya, Tsukasa Browse this author →KAKEN DB
Shime, Hiroaki Browse this author →KAKEN DB
Takaki, Hiromi Browse this author
Azuma, Masahiro Browse this author
Oshiumi, Hiroyuki Browse this author →KAKEN DB
Matsumoto, Misako Browse this author →KAKEN DB
Keywords: RIP signaling
interferon-inducing pathway
Issue Date: Sep-2012
Publisher: Landes Bioscience
Journal Title: OncoImmunology
Volume: 1
Issue: 6
Start Page: 917
End Page: 923
Publisher DOI: 10.4161/onci.21244
Abstract: The engagement of Toll-like receptor 3 (TLR3) leads to the oligomerization of the adaptor TICAM-1 (TRIF), which can induces either of three acute cellular responses, namely, cell survival coupled to Type I interferon production, or cell death, via apoptosis or necrosis. The specific response elicited by TLR3 determines the fate of affected cells, although the switching mechanism between the two cell death pathways in TLR3-stimulated cells remains molecularly unknown. Tumor necrosis factor α (TNFα)-mediated cell death can proceed via apoptosis or via a non-apoptotic pathway, termed necroptosis or programmed necrosis, which have been described in detail. Interestingly, death domain-containing kinases called receptor-interacting protein kinases (RIPs) are involved in the signaling pathways leading to these two cell death pathways. Formation of the RIP1/RIP3 complex (called necrosome) in the absence of caspase 8 activity is crucial for the induction of necroptosis in response to TNFα signaling. On the other hand, RIP1 is known to interact with the C-terminal domain of TICAM-1 and to modulate TLR3 signaling. In macrophages and perhaps tumor cell lines, RIP1/RIP3-mediated necroptotic cell death can ensue the administration of the TLR agonist polyI:C. If this involved the TLR3/TICAM-1 pathway, the innate sensing of viral dsRNA would be linked to cytopathic effects and to persistent inflammation, in turn favoring the release of damage-associated molecular patterns (DAMPs) in the microenvironment. Here, we review accumulating evidence pointing to the involvement of the TLR3/TICAM-1 axis in tumor cell necroptosis and the subsequent release of DAMPs.
Type: article (author version)
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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