Within the Oncomine database, five datasets showed that IL‑17D was significantly decreased in lung cancer, while no dataset showed a significant difference in the expression of IL‑17A, IL‑17B, IL‑17C, IL‑25 or IL17‑F between lung cancer and normal controls.
To investigate the antitumor effect of endostatin in lung cancer, the present study was designed to explore the alterations of microvessel density in Lewis lung cancer models and the expression of vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-17, interferon (IFN)-γ and hypoxia inducible factor (HIF)-1α, following endostatin therapy.
Using a <i>Kras</i>-induced lung cancer mouse model, CC-LR, we previously showed a role for inflammation in lung tumorigenesis through activation of the NF-κB pathway, along with induction of interleukin 6 (IL6) and an IL17-producing CD4<sup>+</sup> T-helper cell response.
In tumors from patients with lung cancer with KRAS mutation we found a correlation between higher levels of IL-17A and colony- stimulating factor 3 and a significant correlation among high neutrophil and lower T-cell numbers.
Polymorphisms of both IL-17A and IL-17F may increase lung cancer risk in Chinese population, and are associated differently with subtypes of clinical-pathologic features and tobacco smoking history of lung cancer patients.
The results indicated high IL-17 expression was independently correlated with poorer OS (HR = 1.82, 95% CI 1.44-2.29, P < 0.00001) and shorter DFS (HR = 2.41, 95% CI 1.42-4.08, P = 0.001) in LC patients.
MSCs significantly augmented lung cancer metastasis, attenuate concentrations of proinflammatory cytokines (TNF-<i>α</i>, IL-17), and increase levels of immunosuppressive IL-10, nitric oxide, and kynurenine in sera of LLC1-treated mice.
Interleukin-17 (IL-17) is a critical pro-inflammatory cytokine, which has been demonstrated to promote development of prostate cancer, colon cancer, skin cancer, breast cancer, lung cancer and pancreas cancer.
As well as the effects of proliferation, apoptosis, migration, and adherent activity of IL-27, IFN-γ, and IL-17 on lung cancer cells were also explored.
To explore the relationship between polymorphisms of interleukin17 (IL-17) gene(A-832G7488A/G) and the susceptibility to silicosis, a risk factor for lung cancer.
Interleukin 17 (IL-17) has been found to be increased in some human cancers; however, the possible implication of IL-17 in regulating antitumor responses in lung cancer patients with malignant pleural effusions (MPE) remains to be elucidated.