This study suggests the need for careful consideration about timing if the application of SOD2 mimetics for prostate cancer therapy is considered.Prostate 76:1338-1341, 2016.
Germline genetic variation in the SOD2 gene might be a predictive biomarker of response to RT for prostate cancer but is not consistently associated with outcome after RT across prostate cancer cohorts with different clinical characteristics.
Here, we performed integrated in vivo and in vitro protocols that analyzed the association between Ala16Val-SOD2 polymorphism and prostate cancer aggressiveness at the time of diagnosis and evaluated the effect of the imbalance on PC proliferation using the DU-145 PC cell line treated with paraquat and porphyrin.
We used Cox proportional hazards regression to examine circulating prediagnostic α-tocopherol, γ-tocopherol, and lycopene; SNPs in SOD2 (n = 5), CAT (n = 6), GPX1 (n = 2), GPX4, (n = 3); and their interactions and risk of lethal prostate cancer among 2,439 men with nonmetastatic prostate cancer in the Health Professionals Follow-up Study and Physicians' Health Study.
In the present study we investigated the association of a number of polymorphic changes in antioxidant system genes (SNPs rs1050450 in the GPX1 gene, rs1695 and rs1138272 in the GSTP1 gene and rs4880 in the MnSOD gene) with the risk of prostate cancer.
Enzyme activities of MnSOD in high-grade PCa tissues were significantly increased but at a lower magnitude compared with the levels of MnSOD protein (0.5-fold vs 2-fold increase).
Statistically significant effect modification of both HCA (DiMeIQx) and darkly browned meat intake and PCa risk was observed for allelic variants of MnSOD (rs4880) (P(interaction): 0.02).
A high tertile selenium level in combination with non-wt rs125701 of the OGG1 gene in combination with smoking status or rs4880 related variation of MnSOD gene appeared to protect from PrCa.
Two variants in SOD2 were significantly associated with the risk of aggressive prostate cancer (rs17884057, odds ratio 0.83, 95% confidence interval 0.70-0.99; and rs4816407, 1.27, 1.02-1.57); men with A alleles at rs2842958 in SOD2 had lower plasma selenium levels (median 116 vs 121.8 µg/L, P= 0.03); and the association between plasma selenium levels and risk of aggressive prostate cancer was modified by SOD1 (rs10432782) and SOD2 (rs2758330).
We identified a genetic variation (G1677T, rs2Y758Y339) in the vicinity of the enhancer region located in intron 2 of the SOD2 gene that creates a potential glucocorticoid responsive element, and developed an assay to screen DNA samples of 220 individuals (73 control, 59 prostate cancer survival individuals and 88 lung cancer biopsies).
These data suggest that the relationship between circulating selenium levels at diagnosis and prognostic risk of prostate cancer is modified by SOD2 genotype and indicate caution against broad use of selenium supplementation for men with prostate cancer.
To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility.
Association of single nucleotide polymorphisms in SOD2, XRCC1 and XRCC3 with susceptibility for the development of adverse effects resulting from radiotherapy for prostate cancer.
The results of our study of Turkish prostate cancer patients suggest that mutation of the MnSOD gene may be an important risk factor for prostate cancer.
These results suggest that the Ala variant of SOD2 is associated with moderately increased risk of prostate cancer, particularly among men with lower intakes of dietary and supplemental vitamin E.
In conclusion, it does not seem that variants in MnSOD, CAT, or GPX1 have an influence on prostate cancer risk in this cohort of men who were smokers or exposed to asbestos, although it is possible that cumulative defects in protection from oxidative stress may result in increased risk of the disease.
Here we investigated the role of the SOD2 polymorphism in: a) age-related mortality, b) morbidity (breast and prostate cancer), c) immunological markers, and d) DNA damage in peripheral blood cells.
CDNA expression array analysis revealed increased manganese superoxide dismutase (SOD-2) expression in the mac25/IGFBP-rP1-transfected M12 human prostate cancer cell line compared to M12 control cells.