Table 1.
Pro- or anti-tumoral effects mediated by TLRs.
Receptor | Tumor Type | Tumor Role | Mechanism | Pathways or Molecules Involved | Ref |
---|---|---|---|---|---|
TLRs | Intestine, liver, skin | Protumoral | Inflammation | NF-κB, IL-1β, TNFα and IL-6 | [46] |
TLR2 | Gastric | Protumoral | Cell survival and proliferation in gastric tumor epithelium | PI3K/Akt, ERK1/2, JNK MAPKs, NF-kb | [47] |
TLR2/6 | Lewis lung carcinoma | Protumoral | Inflammation, macrophage activation, metastasis | Myd88, TRIF, ECM-protein versican, IL-6, TNF-α | [48] |
TLR2/4 | Lung | Protumoral | ECM remodeling, | EGFR | [38] |
TLR3 | Breast | Protumoral | Tumor growth | β- Catenin, NF-κB | [49] |
TLR4 | Liver | Protumoral | Inflammation | NF-κB | [50] |
TLR4 | Lung | Protumoral | immunosuppression, antiapoptosis | VEGF, TGF-β, IL-8 | [42] |
TLR4 | Colon | Protumoral | Inflammation, tumor burden | Cox-2 | [51] |
TLR4 | Skin | Protumoral | Inflammation | Myd88 | [52] |
TLR7 | Pancreatic | Protumoral | Stromal inflammation | NF-kB, MAPKs | [53] |
TLR7, TLR8 | Lung | Protumoral | Inflammation, tumor cell growth and survival, chemoresistance | NF-kB, MAPK, IRF, Bcl-2, IL-6, IL-8, CSF-2, IL-1α, IL-12, NOS-2 | [44] |
TLR9 | Lung | Protumoral | Monocyte recruitment, antiapoptosis | MCP1 | [45] |
TLR2 | Lung | Antitumoral | Monocytic myeloid-derived suppressor cell | JNK, TNF-α, IL-12p40, IL-12p70 | [54] |
TLR3 | Prostate, liver | Antitumoral | Treatment with agonist stops tumor growth | Type I interferons | [55] |
TLR3 | Liver | Antitumoral | Induction of tumor parenchyma (hepatocytes) cell death; induction of intratumor expression of chemokines that attract NK cells or T cells to the tumor microenvironment; and activation of tumor-infiltrating NK cells that promote cytotoxic activity. | IFN-γ | [56] |
TLR5 | Breast, colon | Antitumoral | Immune cell activation | Dendritic cells | [37,57,58] |
TLR7/8 | Melanoma | Antitumoral | Immune cell activation | Dendritic cells and Natural Killer | [38,39] |