Abstract
The HOGG1 gene catalyzes the excision of modified bases and removal of DNA damage adducts. It may play an important role in the prevention of carcinogenesis. Ser326Cys polymorphism localizes in exon 7 of the hOGG1 gene. It takes the form of an amino acid substitution, from serine to cysteine, in codon 326. Several epidemiological association studies have been conducted on this polymorphism and its relationship with the risk of prostate cancer. However, results have been conflicting. To resolve this conflict, we conducted a meta-analysis on the association between this polymorphism and prostate cancer, taking into account race, country, sources of controls, and smoking status. A total of nine studies covering 2779 cases and 3484 controls were included in the current meta-analysis. Although no significant association was found between hOGG1 Ser326Cys polymorphism and prostate cancer susceptibility in the pooled analysis, individuals with Ser/Cys+Cys/Cys genotypes were found to have greater risk of prostate cancer if they were also smokers (OR = 2.66, 95% CI = 1.58−4.47) rather than non-smokers (OR = 2.18, 95% CI = 1.13−4.19), compared with those with Ser/Ser genotype. In conclusion, our meta-analysis demonstrates that hOGG1 Ser326Cys polymorphism is a risk factor for prostate cancer in smokers. Further studies are needed to confirm this relationship.
Highlights
Oxidative DNA damage is involved in carcinogenesis
A DNA glycosylase/apurinic-apyrimidinic lyase encoded by the human oxoguanine glycosylase 1 gene catalyzes the excision of modified bases and removal of 8OH-dG adducts and has been hypothesized to play an important role in the prevention of carcinogenesis [2]
The potential role of human oxoguanine glycosylase 1 (hOGG1) Ser326Cys polymorphism as a determinant of prostate cancer risk was investigated in a sample of 6263 subjects from nine published case-control studies
Summary
Oxidative DNA damage is involved in carcinogenesis. The major form of DNA adduction induced by oxidative damage is 8-OH-dG (8-hydroxy-2-deoxyguanine) and increased 8-OH-dG formation in DNA results in mutagenesis and carcinogenesis [1]. A DNA glycosylase/apurinic-apyrimidinic lyase encoded by the human oxoguanine glycosylase 1 (hOGG1) gene catalyzes the excision of modified bases and removal of 8OH-dG adducts and has been hypothesized to play an important role in the prevention of carcinogenesis [2]. Prostate cancer is most commonly-diagnosed malignancy in elderly men in developed countries, and the incidence increases every year. Deficient DNA repair mechanisms may play a role in the age-related increase in prostate cancer risk by allowing carcinogenic DNA damage events to accumulate uncorrected. Higher levels of 8-OH-dG and downregulation of hOGG1 have been observed in benign prostatic hyperplasia (BPH) and prostate cancer
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