Table 1.
IL-17B IL-17RB expression in cancers.
| Tumor | Expression—Prognosis | Mechanism—Models | References |
|---|---|---|---|
| Breast | IL-17RB upregulation is correlated with poor prognosis. | ShRNA-dependent reduction of IL-17B decreases tumor growth and invasiveness of MDA-MB468 human breast cancer cells. | (27) |
| Breast | IL-17RB upregulation is correlated with poor prong/osis. | IL-17RB recruits TRAF6, activates NF-kB, upregulates Bcl-2, and induces resistance to etoposide. IL-17RB or IL-17B targeting with Abs attenuates human MDA-MB361 breast cancer cell colony formation in vitro and tumor growth in vivo. |
(28) |
| Breast | High expression of IL-17B and IL-17RB is associated with poor prognosis. IL-17B upregulation is associated with poorer survival in patients with basal-like breast cancer. |
MCF7 and MDA-MB468 human breast cancer cells that overexpress IL-17B are resistant to paclitaxel. Treatment with anti-IL-17RB antibodies restores breast tumor chemosensitivity in vivo. |
(10) |
| Breast | TGF-β secreted by Treg cells up-regulates IL-17RB on 4T1 and EMT6 murine breast cancer cells via Smad2/3/4 signaling and increases their tumor growth and metastatic potential in vivo. | (29) | |
| Pancreas | IL-17RB overexpression is associated with metastasis and poor clinical outcome. | Depletion of IL-17B or IL-17RB by shRNA or treatment with anti-IL-17B or anti-IL-17RB antibodies reduces CFPAC-1 and BxPC3 pancreatic cell line colony formation, invasion, tumor growth, and metastasis in xenograft models. | (11) |
| Gastric | IL-17RB expression in group 2 innate lymphoid cells (ILC2) is higher in peripheral blood mononuclear cells from patients with gastric cancer than in healthy donors. | IL-17RB expression by ILC2. | (30) |
| Gastric | Overexpression of IL-17RB correlates with poor prognosis. IL-17B level in serum is higher in patients with gastric cancer than in healthy donors. |
IL-17B activates the AKT/β-catenin pathway and promotes stemness and EMT of MGC-803 human gastric cancer cells. | (31) |
| Glioblastoma | A signature with 6 enriched cytokines (incl. enriched expression of IL-17B) predicts poor overall survival | (32) | |
| Primary testicular lymphoma | A signature with 25 enriched cytokines (including IL-17B) predicts poor survival. | (33) | |
| Colon | IL-17B expression is increased in moderate and poorly differentiated tumors. | IL-17RB is expressed by colon epithelial cells. Neutrophils are the main source of IL-17B in the stroma. |
(34) |
| Prostate | IL-17RB expression is higher in cancer-associated fibroblasts from prostate cancer patients than in fibroblasts from benign prostate hyperplasia. | IL-17RB expression by cancer-associated fibroblasts. | (35) |
| ATL | Overexpression of IL-17RB in leukemic cells. | Tax induces IL-17RB expression in a NF-kB dependent-manner in the HTLV-1 transformed T cell lines C8166 and MT-2. | (36) |
| Thyroid | IL-17RB is upregulated in thyroid cancer tissues compared with normal thyroid tissues. | IL-17B/IL-17RB signaling induces ERK activation, MMP-9 expression and promotes migration and invasion of SW1736 thyroid cancer cells. IL-17RB signaling contributes to tumor growth and metastasis formation of SW1736 tumor cell xenografts. |
(37) |
| Lung | High IL-17B expression is associated with poor overall survival. High IL-17RB expression is associated with positive lymph nodes and distant metastases and positive distant metastases, and is predictive of disease-free survival and overall survival. |
IL-17RB expression positively correlates with the invasion potential of lung cancer cell lines. IL-17RB promotes invasion/migration of H441 lung carcinoma cells through activation of the ERK signaling pathway, and its overexpression increases their metastatic potential in vivo. |
(12) |
| AML | IL-17B and IL-17RB mRNA expression is significantly upregulated in patients with AML. | IL-17B/IL-17RB signaling drives MOLM-13 AML cell resistance to Ara-C (ERK/NF-kB/Bcl-2). Ara-C increases IL-17B expression. |
(38) |