Journal
MEDICINA-LITHUANIA
Volume 58, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/medicina58101414
Keywords
reactive oxygen species; oxidative stress; antioxidant enzymes; prostate cancer; SNP
Categories
Funding
- Ministry of Education, Science and Technological Development of the Republic of Serbia [200110]
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The study suggests that genetic polymorphisms of antioxidant enzymes GPX1, SOD2, and regulatory protein Nrf2 may increase the risk of prostate cancer development. Carriers of SOD2*C allele have an increased risk, which is further amplified when combined with Nrf2*C/C genotype. The study highlights the importance of acquired contributory factors in the risk of prostate cancer.
Background and Objectives: Mounting evidence implicates oxidative damage in prostate carcinogenesis, contributing to modifications of macromolecules that drive cellular malignant transformation. Functional single-nucleotide polymorphisms (SNPs) of enzymes involved in redox homeostasis can disrupt pro-oxidant-antioxidant balance, leading to accumulation of reactive oxygen species and oxidative damage. We investigated the potential role of genetic polymorphisms of antioxidant enzymes glutathione peroxidase 1 (GPX1 rs1050450) and superoxide dismutase 2 (SOD2 rs4880) and regulatory antioxidant protein nuclear factor erythroid 2-related factor 2 (Nrf2 rs6721961) in the susceptibility to prostate cancer development (PC) and prognosis. Materials and Methods: We conducted a case-control study consisting of 235 patients with PC and 240 controls. Gene polymorphisms were determined by quantitative polymerase chain reaction (qPCR) and polymerase chain reaction with confronting two-pair primers (PCR-CTTP) methods. Multiple risk models were composed to inspect the separate and mutual effect of multiple genes and in combination with acquired contributory factors on the risk of PC development. Results: Independently, carriers of at least one SOD2*C allele had increased risk of PC development, which was significantly further amplified in advanced statistical models. When tested in combination, individuals with both SOD2*C allele and Nrf2*C/C genotype were also at increased risk of PC development, which was augmented when combined with acquired contributory factors. During the mean 75 +/- 25 months of follow-up, investigated gene polymorphisms did not affect overall survival. Conclusion: Our results suggest that these gene polymorphisms could be used as risk biomarkers of PC evolution.
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