Abstract
Background/Aims: Previous results on the association between MTR gene A2756G polymorphism and PCa risk are inconclusive.Methods: We used odds ratios (ORs) with corresponding 95% confidence intervals (95% CIs) to evaluate the correlation between MTR A2756G polymorphism and risk of PCa in meta-analysis. Serum expression of MTR was detected by ELISA and in-silico tools were utilized to assess this variant.Results: Our study included 2,921 PCa patients and 3,095 control subjects. The results indicated that the MTR A2756G polymorphism is linked with an increased risk of PCa using three genetic models (G-allele vs. A-allele: OR = 1.16, 95%CI = 1.04 - 1.30; GA vs. AA: OR = 1.17, 95%CI = 1.02 - 1.33; GG+GA vs. AA: OR = 1.18, 95%CI = 1.04 - 1.34). Stratified analysis produced similar results. A significant association was also indicated in advanced PCa from the meta-analysis. Finally, our experiments showed evidence that serum MTR levels in PCa patients with AA genotypes were statistically higher than in those with GG/GA genotypes.Conclusions: Our present study suggests that the MTR A2756G polymorphism may contribute to the risk of developing PCa, particularly in Asian and hospital-based studies. Moreover, serum MTR might be utilized in diagnosis of PCa.
Highlights
Prostate cancer (PCa) remains the most common carcinoma in males and the sixth leading cause of tumor-associated deaths in Western countries [1]
A total of 7 articles containing 2,921 PCa patients and 3,095 control subjects concerning the MTR A2756G polymorphism were enrolled in our meta-analysis
Previous research has shown evidence that some risk factors, including ethnicity, toxins, lifestyle, single nucleotide polymorphism (SNP), and family history may contribute to the process and development of PCa [27,28,29]
Summary
Prostate cancer (PCa) remains the most common carcinoma in males and the sixth leading cause of tumor-associated deaths in Western countries [1]. Previous studies have indicated that folate-metabolizing genes play a significant role in carcinogenesis through DNA methylation [9,10,11]. Published epidemiological studies have been performed to test whether the MTR A2756G (rs1805087) variant is associated with PCa risk; the results remain inconsistent rather than conclusive [17,18]. We performed an updated meta-analysis with accumulated data from all eligible researches to enhance the statistical powers of previous studies and ascertain precise correlation between the MTR variant and PCa risk. We enrolled 200 newly diagnosed PCa patients in our centers and investigated the serum expression of MTR by ELISA and utilized in-silico tools to confirm the results of our meta-analysis
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