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| Substrate | Role in cancer | Role in inflammation |
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| MERTK [108] | MERTK inhibition via monoclonal antibodies, ligand traps, or small molecule tyrosine kinase inhibitors can reverse pro-oncogenic phenotypes [171]. | Cleavage-resistant mutants of MERTK have less lung injury and inflammation in a reperfusion injury model [109]. |
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| Toll-like receptor 2 (TLR2) [114] | In a cancer model, mice lacking TLR2 had smaller stomachs, smaller gastric tumors, and fewer gastric lesions compared with control mice. Also, injection of a TLR2-blocking antibody into mice reduced stomach size and tumor burden using mice with gastric cancer [111]. | TLR2−/− mice compared with TLR2+/+ animals, using a model of progressive renal injury, had reduced inflammation and influx of neutrophils and production of chemokines and TGFβ in kidneys [112]. |
| In a diabetic wound model, the absence of TLR2 results in decreased inflammation and improved wound healing [113]. |
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| Syndecan-1 (SDC1) [56] | Soluble SDC1 is correlated with a poor prognosis and resistance to many chemotherapeutic agents [117]. | In a mouse model of bleomycin-induced acute lung injury, SDC1 shedding attenuates lung injury [118]. |
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| Insulin growth factor 1 receptor (IGF1R) [121] | Increased IGF1R expression has been reported in several cancers [172, 173]. NT157, which targets IGF1R, reduces tumor burden [119]. | IGF-1, through binding to IGF1R, is a suppressor of the immune system and has been used in experimental models of multiple sclerosis [120]. |
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| Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) [124] | LRIG1, human EGFR inhibitor, reverses multidrug resistance [174]. | LRIG1 is a negative regulator of the STAT3-dependent inflammatory pathway [125]. |
| Adenovirus-mediated LRIG1 expression enhances the chemosensitivity of bladder cancer cells to cisplatin [123]. |
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