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Interleukin-17 (IL-17), a proinflammatory cytokine, mainly produced by Th17 cells, participates in both innate and adaptive immune responses and is involved in various diseases, including infectious diseases, autoimmune disorders and cancer. Emerging evidence indicates that IL-17 not only has an oncogenic role in tumorigenesis by regulating tumor angiogenesis and enhancing tumor immune evasion but also exerts anti-tumor functions by enhancing natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) activation and through the recruitment of neutrophils, NK cells and CD4 + and CD8 + T cells to tumor tissue. In this review, we provide an overview on the basic biology of IL-17 and recent findings regarding its enigmatic double-edged features in tumorigenesis, with special attention to the roles of IL-17 produced by tumor cells interacting with other factors in the tumor microenvironment. [ABSTRACT FROM AUTHOR]

Abstract: Published data on the association between miR-196a2 T/C polymorphism and cancer susceptibility are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. A total of 21 studies including 10,441 cases and 12,353 controls were involved in this meta-analysis. Overall, significantly elevated cancer risk was associated with miR-196a2 C allele when all studies were pooled into the meta-analysis (TC vs. TT: OR=1.23, 95% CI=1.11–1.36; CC vs. TT: OR=1.30, 95% CI=1.14–1.48; dominant model: OR=1.25, 95% CI=1.13–1.38). In the subgroup analysis by ethnicity, significantly increased risks were found in Asains (TC vs. TT: OR=1.24, 95% CI=1.10–1.40; CC vs. TT: OR=1.31, 95% CI=1.13–1.52; dominant model: OR=1.26, 95% CI=1.12–1.41) but with bordline statistical significance in Caucasians (TC vs. TT: OR=1.15, 95% CI=1.00–1.31). In the subgroup analysis by cancer type, statistically significantly increased risks were found for breast cancer (TC vs. TT: OR=1.15, 95% CI=1.01–1.31; CC vs. TT: OR=1.30, 95% CI=1.01–1.68; dominant model: OR=1.22, 95% CI=1.00–1.50; and recessive model: OR=1.11, 95% CI=1.01–1.23) and lung cancer (CC vs. TT: OR=1.30, 95% CI=1.10–1.54; and recessive model: OR=1.18, 95% CI=1.02–1.36). When stratified by study design, statistically significantly elevated risk was found in hospital-based studies (TC vs. TT: OR=1.30, 95% CI=1.13–1.49; CC vs. TT: OR=1.37, 95% CI=1.14–1.66; dominant model: OR=1.32, 95% CI=1.15–1.53) and population-based studies (CC vs. TT: OR=1.19, 95% CI=1.06–1.35; dominant model: OR=1.13, 95% CI=1.01–1.25). Despite some limitations, this meta-analysis suggests that the miR-196a2 C allele is a low-penetrant risk factor for cancer development. [Copyright &y& Elsevier]