Table 1: Role of IL-17 in CRC.

SpeciesMediatorsFindingsReferences

Tumor promoting role
HumanVEGFIL-17 induces both CRC cell lines and primary cancer cells to produce VEGF.[52]

HumanHIF-1 and c-mycIL-17 and TNF cooperatively stimulate glycolysis in CRC cells via induction of HIF-1 and c-myc expression.[45]

MouseStat 3IL-23/IL-17 signaling activated by microbial products promotes STAT3 phosphorylation in CRC epithelial cells.[48]

MouseVEGF, KC, and PGE2IL-17 promotes angiogenesis via induction of a variety of proangiogenic factors secretion from fibroblasts and tumors.[36]

MouseIL-6, IL-23, and IL-1 ;
KC and Cox-2;
CD4 T cells
IL-6, IL-23, IL-1 , KC, and Cox-2 are decreased and function of CD4 T cells alters in ApcMin/+ mice, resulting in abrogating spontaneous intestinal tumorigenesis.[17]

MouseIL-6, STAT3, and TNF- ;
cyclin D1, cyclin-dependent kinase 2, and cyclin E
IL-17A knockout decreases IL-6, STAT3, TNF- , cyclin-D1, cyclin-dependent kinase 2, and cyclin E and inhibits CAC tumorigenesis.[46]

Mouse G-CSF, VEGF, and Bv8
NF- B and ERK signaling
IL-17 induces the expression of G-CSF through NF- B and ERK signaling, enhancing proangiogenic function via VEGF and Bv98 and promoting tumor growth. [50]

Tumor inhibiting activity
MouseIFN-
NK cells and T cells
IL-17-deficient decreases IFN- NK and tumor-specific IFN- T cells and promotes tumor growth and lung metastasis.[53]

HumanClaudin
ERK MAPK pathway
IL-17 enhances the development of the tight junctional barrier mediated by claudin of T84-cell monolayers via ERK MAPK pathway in intestine.[54]