Research Paper Volume 12, Issue 1 pp 825—843
Association between SOD2 V16A variant and urological cancer risk
- 1 Department of Urology, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou 213003, China
- 2 Department of Oncology, Taizhou People's Hospital, Taizhou 225300, China
- 3 Department of Cardiology, Taizhou People's Hospital, Taizhou 225300, China
- 4 Department of Urology, Affiliated Hospital of Jiangnan University, Wuxi 214000, China
received: September 9, 2019 ; accepted: December 24, 2019 ; published: January 12, 2020 ;https://doi.org/10.18632/aging.102658
How to Cite
Copyright © 2020 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: The correlation between superoxide dismutase 2 (SOD2) V16A variant and urological cancer susceptibility has been widely studied, however, with divergent results.
Results: Totally, 9,910 cancer patients and 11,239 control subjects were enrolled. V16A variant is associated with an increased susceptibility to urological cancer (A-allele vs. V-allele: OR = 1.06, 95% CI = 1.00 – 1.13, P = 0.047; AA+AV vs. VV: OR = 1.09, 95% CI = 1.02 – 1.16, P = 0.008), especially for prostate cancer (PCa). Serum SOD2 level of PCa patients with VV+VA genotypes was lower than in those with AA genotypes. SOD2 expression is downregulated in both prostate and bladder cancer, as compared to the control. Furthermore, SOD2 was found to be downregulated in more advanced PCa participants, as compared to the ones in early stages. PCa subjects with low SOD2 expression displayed a shorter disease-free survival (DFS) time compared to that of the high SOD2 expression counterparts.
Conclusions: The SOD2 V16A variant may be associated with increased urological cancer susceptibility, especially for prostate cancer.
Methods: A pooled analysis utilizing odds ratios (ORs), in silico tools and ELISA was adopted to demonstrate this association. We also used immunohistochemical staining (IHS) to assess SOD2 expression.
AKT1: RAC-alpha serine/threonine-protein kinase; BCa: bladder cancer; CAT: Catalase; CFB: complement factor B; ELISA: enzyme linked immunosorbent assay; FOXO3: Forkhead box protein O3; GPX1: Glutathione peroxidase 1; HB: hospital-based; HWE: Hardy-Weinberg equilibrium of controls; IHS: immunohistochemical staining; MS: Mass spectrometry; NA: not available; PB: population-based; PCa: prostate cancer; PCR-RFLP: polymerase chain reaction and restrictive fragment length polymorphism; RCC: renal cell carcinoma; RT: real time; SOD2: superoxide dismutase 2; SIRT3: NAD-dependent protein deacetylase sirtuin-3.