Interleukin-17 (IL-17) is a proinflammatory cytokines produced by T helper 17 (Th17) cells, which plays an important role in both innate and adaptive immune systems. Genetic variants in the IL-17 genes may influence the immunopathogenesis of many cancers. In our study, we investigated the association of three single-nucleotide polymorphisms (SNPs: -152 G/A, 7488 A/G and 7383 A/G) in the IL-17A and IL-17F genes with lung cancer risk, in the Tunisian population. The genotypic and allelic distributions of IL-17A and IL-17F genes polymorphisms were analyzed by Polymerase Chain-Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) for 239 patients and 258 healthy controls. Our results revealed a statistically significant association between IL-17F 7488G allele and increased lung cancer risk (P=0.028). Stratification analysis indicated that IL-17F 7488G allele enhances the risk of lung cancer development among men and oldest age subject groups (P<0.05). Patients with IL-17F 7488G allele were also more likely to be diagnosed at advanced stage (P=0.04), or with metastatic lung cancer (P=0.035). Furthermore, no significant association between IL-17F 7383 A/G, IL-17 -152G/A polymorphisms and lung cancer risk was observed (P>0.05). However, we reported contradictory findings on the association of IL-17 -152 G/A polymorphisms with lung cancer risk. In addition, we suggested the existence of a biological interaction between IL-17A, but not IL-17F polymorphisms and smoking. Our findings suggest that IL-17F 7488G allele is associated with increased lung cancer risk in the Tunisian population.
Keywords: Biological interaction; Interleukin-17; Lung cancer; Polymorphisms; Restriction fragment length polymorphism.
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