Ten interleukins and risk of prostate cancer

BackgroundInterleukins (ILs) have been reported to be related to prostate cancer. The aims of this study were to estimate the levels for several key interleukins in prostate cancer and the causal effects between them. MethodsWe conducted a bi-directional two-sample Mendelian randomization (MR) study to assess the causal associations between ILs and prostate cancer. Genetic instruments and summary-level data for 10 ILs were obtained from three genome-wide association meta-analyses. Prostate cancer related data were obtained from the PRACTICAL (79,148 cases and 61,106 controls), UK Biobank (7,691 cases and 169,762 controls) and FinnGen consortium (10,414 cases and 124,994 controls), respectively. ResultsThe odds ratio of prostate cancer was 0.92 (95% confidence interval (CI), 0.89, 0.96; P=1.58x10(-05)) and 1.12 (95% CI, 1.07, 1.17; P=6.61x10(-07)) for one standard deviation increase in genetically predicted IL-1ra and IL-6 levels, respectively. Genetically predicted levels of IL-1ss, IL-2a, IL-6ra, IL-8, IL-16, IL-17, IL-18, and IL-27 were not associated with the risk of prostate cancer. Reverse MR analysis did not find the associations between genetic liability to prostate cancer and higher levels of IL-1ra (beta, -0.005; 95% CI, -0.010, 0.001; P=0.111) and IL-6 (beta, 0.002; 95% CI, -0.011, 0.014; P=0.755). ConclusionThis MR study suggests that long-term IL-6 may increase the risk of prostate cancer and IL-1ra may reduce it.

Automated summary

This study used Mendelian randomization to investigate the causal associations between interleukins (ILs) and prostate cancer. The results indicate that long-term exposure to IL-6 may increase the risk of prostate cancer, while IL-1ra may reduce the risk.