Studies have shown that 48.59% of benign prostate hyperplasia (BPH) is combined with metabolic syndrome (MetS). The mainstream view supports the correlation between MetS and BPH, but the pathogenesis of MetS-BPH is not fully understood. Four hundred and seventy-four men, aged 47 years or older, were recruited into this study by consecutive routine physical examination programs, and several parameters were obtained from each participant. Based on the diagnosis of BPH, MetS, and MetS-BPH, the participants were divided into BPH and Non-BPH groups, MetS and Non-MetS groups, as well as MetS-BPH and Non-MetS-BPH groups. The values of the obtained parameters were evaluated using Student's t-test, chi-square test, and logistic regression analysis. The value of estradiol (E2) was higher in the diseased groups (BPH, MetS, and MetS-BPH groups) compared with the corresponding control groups (Non-BPH, Non-MetS, and Non-MetS-BPH groups), and the differences were statistically significant. Also, E2 had an independent association with BPH (OR = 2.286, 95% CI: 1.723-3.593, p < 0.001), MetS (OR = 1.406, 95% CI: 0.585-2.315, p < 0.001), and MetS-BPH (OR = 1.249, 95% CI: 0.795-1.962, p < 0.001). Regarding SNPs of CYP19A1 gene, both the rs4646 genotypes (CC, CA, and AA) and the rs700518 genotypes (CC, CT, and TT) were present in every group, and all genotypes had statistically significant differences between the diseased and corresponding control groups. However, only the TT genotype of rs700518 was independently associated with BPH, MetS, and MetS-BPH after adjusting for age. The TT genotype of rs700518 is an independent risk factor for the MetS-BPH populations, and the CYP19A1 gene regulation of estrogen leads to MetS-BPH.

ABSTRACT. Strong evidence suggests that cancer-associated inflammation promotes tumor growth and progression, and interleukin-6 (IL6) is an important modulator of inflammation. However, the roles of IL6 and mutations of its corresponding gene in prostate cancer have not been clearly documented. We retrieved data from the Oncomine database concerning IL6 expression in prostate cancer and its role in prostatespecific antigen (PSA) recurrence. We also performed a case-control study of the IL6 -572G/C polymorphism (rs1800796) in 236 sporadic prostate cancer patients and 256 healthy controls from a southern Han Chinese population. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between rs1800796 and prostate cancer susceptibility. A dual-luciferase reporter assay was used to test the transcriptional activity of the IL6 promoter G and C alleles. IL6 was overexpressed in prostate cancer tissues compared to normal tissues, especially in those with higher Gleason scores. Moreover, elevated IL6 expression was associated with high PSA recurrence rate in Oncomine data. Our case-control study demonstrated that compared with the -572C allele, the -572G allele conferred a borderline increased risk of prostate cancer (OR = 1.31, 95%CI = 0.99-1.74, P = 0.061). This was more pronounced in the subgroup of individuals having never smoked (OR = 1.85, 95%CI = 1.07-3.22). Moreover, the G allele showed increased activity relative to the C allele in the dual-luciferase reporter assay. Our results suggest that the -572G/C polymorphism may be associated with IL6 expression, which in turn plays a role in prostate cancer development.