Table 1.
Role of IL-17 in CRC.
Species | Mediators | Findings | References |
---|---|---|---|
Tumor promoting role | |||
Human | VEGF | IL-17 induces both CRC cell lines and primary cancer cells to produce VEGF. | [52] |
| |||
Human | HIF-1α and c-myc | IL-17 and TNFα cooperatively stimulate glycolysis in CRC cells via induction of HIF-1α and c-myc expression. | [45] |
| |||
Mouse | Stat 3 | IL-23/IL-17 signaling activated by microbial products promotes STAT3 phosphorylation in CRC epithelial cells. | [48] |
| |||
Mouse | VEGF, KC, and PGE2 | IL-17 promotes angiogenesis via induction of a variety of proangiogenic factors secretion from fibroblasts and tumors. | [36] |
| |||
Mouse | IL-6, IL-23, and IL-1β; KC and Cox-2; CD4 T cells |
IL-6, IL-23, IL-1β, KC, and Cox-2 are decreased and function of CD4 T cells alters in ApcMin/+ mice, resulting in abrogating spontaneous intestinal tumorigenesis. | [17] |
| |||
Mouse | IL-6, STAT3, and TNF-α; cyclin D1, cyclin-dependent kinase 2, and cyclin E |
IL-17A knockout decreases IL-6, STAT3, TNF-α, cyclin-D1, cyclin-dependent kinase 2, and cyclin E and inhibits CAC tumorigenesis. | [46] |
| |||
Mouse | G-CSF, VEGF, and Bv8 NF-κB and ERK signaling |
IL-17 induces the expression of G-CSF through NF-κB and ERK signaling, enhancing proangiogenic function via VEGF and Bv98 and promoting tumor growth. | [50] |
| |||
Tumor inhibiting activity | |||
Mouse | IFN-γ
NK cells and T cells |
IL-17-deficient decreases IFN-γ + NK and tumor-specific IFN-γ + T cells and promotes tumor growth and lung metastasis. | [53] |
| |||
Human | Claudin 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] |