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TLR signaling in cancers
Jong-Hwan Park
Department of Biochemistry, College of Medicine, Konyang University, Daejeon, 302-718
Republic of Korea
Toll-like receptors (TLRs) are type Ⅰ transmembrane receptors that recognize conserved
molecular patterns of microbial origin. Extracellular surface TLRs including TLR2, TLR4,
and TLR5 recognize bacterial lipoproteins, lipopolysaccharide (LPS), and flagellin,
respectively, whereas endosomal TLRs such as TLR3, TLR7/8, and TLR9 sense dsRNA,
ssRNA, and CpG motif from bacterial and viral DNA. TLR activation with their specific
ligands leads to NF-κB, mitogen-activated protein kinases (MAPKs) or interferon regulatory
factors (IRFs) activation through myeloid differentiation factor 88 (MyD88)-dependent and
MyD88- independent [TIR domain-containing adaptor protein inducing interferon β (TRIF)dependent] pathway and subsequently produce proinflammatory cytokines or type Ⅰ
interferons. Although TLR signaling has been extensively studied in innate immune response
against microbial infection, plenty of recent studies have uncovered its role on tumor
development. TLR signaling is involved in not only tumor progression by promoting cell
proliferation, migration, invasion, and angiogenesis, but also in tumor suppression by
inducing cell death or immune activation. These events critically depend on tumor origin or
TLR type. In this study, we discussed the function of TLRs on tumor development such as
cell proliferation, metastasis, and immune suppression.