Interplay between Inflammation and Stemness in Cancer Cells: The Role of Toll-Like Receptor Signaling

Figure 1

TLR and the related TNFR and IL-1R signaling pathways. TLRs utilize a MYD88 dependent pathway (black line) and a TRIF dependent pathway (blue line) to activate NF-κB, AP-1, and IRF3, leading to the production of inflammatory cytokines and type I interferons. IL-1R uses the same set of signaling molecules, and TNFR utilizes the same signaling pathway as TLRs. TLR, toll-like receptor; IL-1R, interleukin-1 receptor; TNFR, tumor necrosis factor receptor; LPS, lipopolysaccharide; TRADD, TNFRSF1A associated via death domain; TIRAP, TIR domain containing adaptor protein; RIP, receptor interacting serine/threonine kinase; IRAK, interleukin-1 receptor associated kinase; TRAF2, TNF receptor associated factor 2; TRAF3, TNF receptor associated factor 3; TRAF6, TNF receptor associated factor 6; TAK1, TGF-beta activated kinase 1; MAPK, mitogen-activated protein kinase 1; IKK, I-kappa B kinase; IκB, NFKB inhibitor; Tab2, TGF-beta activated kinase 1 binding protein 2; TBK1, TANK-binding kinase 1; MYD88, myeloid differentiation primary response 88; TRIF, TIR domain containing adapter-inducing interferon-β; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; AP-1, activator protein 1; IRF3, interferon regulatory factor 3.