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Mn-SOD and CuZn-SOD polymorphisms and interactions with risk factors in gastric cancer

World Journal of Gastroenterology 2010年第37期16卷 4738-4746页

作者： Jian-Feng Yi Shi-Liang Kang Xiang-Ting Zeng Yu-Min Li Tao Liu Jun-Qiang Zhang Wen-Ting He Xun Li Wen-Ce Zhou The First College of Clinical Medicine of Lanzhou University Lanzhou 730000 Gansu Province China Key Laboratory of Digestive System Tumors Lanzhou University Second Hospital China Department of General Surgery The Fir st Hospital of Lanzhou Unive rsityLanzhou 730000Gansu ProvinceChina

AIM: To investigate the effects of superoxide dismutase (SOD) polymorphisms (rs4998557 , rs4880), Helicobacter pylori (H. pylori ) infection and environmental factors in gastric cancer (GC) and malignant potential of gastric precancerous lesions (GPL). METHODS: copper-zinc superoxide dismutase (SOD1, CuZn-SOD)-G7958A (rs4998557 ) and manganese superoxide dismutase (SOD2, Mn-SOD)-Val16Ala (rs4880 ) polymorphisms were genotyped by SNaPshot multiplex polymerase chain reaction (PCR) in 145 patients with GPL (87 cases of gastric ulcer, 33 cases of gastric polyps and 25 cases of atrophic gastritis), 140 patients with GC and 147 healthy controls. H. pylori infection was detected by immunoblotting analysis. RESULTS: The SOD1-7958A allele was associated with a higher risk of gastric cancer [odds ratio (OR) = 3.01, 95% confidence intervals (95% CI): 1.83-4.95]. SOD216Ala/Val genotype was a risk factor for malignant potential of GPL (OR = 2.04, 95% CI: 1.19-3.49). SOD216Ala/genotype increased the risk of gastric cancer (OR = 2.85, 95% CI: 1.66-4.89). SOD1-7958A/genotype, SOD2-16Ala/genotype, alcohol drinking, positive family history and type Ⅰ H. pylori infection were associated with risk of gastric cancer, and there were additive interactions between the two genotypes and the other three risk factors. SOD2-16Ala/Val genotype and positive family history were associated with malignant potential of GPL and jointly contributed to a higher risk for malignant potential of GPL (OR = 7.71, 95% CI: 2.10-28.22). SOD1-7958A/genotype and SOD2-16Ala/genotype jointly contributed to a higher risk for gastric cancer (OR = 6.43, 95% CI: 3.20-12.91). CONCLUSION: SOD1-7958A/and SOD2-16Ala/-genotypes increase the risk of gastric cancer in Chinese Han population. SOD2-16Ala/-genotype is associated with malignant potential of GPL.

关键词： copper-zinc superoxide dismutase Manganese superoxide dismutase Gastric cancer Gastric precancerous lesions Gene polymorphisms Interaction

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SUMO-1 modification increases human SOD1 stability and aggregation

SUMO-1 modification increases human SOD1 stability and aggre...

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华东六省一市生物化学与分子生物学学会2006年学术交流会

作者： Erkang Fei, Nali Jia, Hongfeng Wang, Tao Zhang, Xiaochuan Ma, and Guanghui Wang (School of Life Sciences,University of Science & Technology of China,Hefei, Anhui 230027, People’s Republic of China)

The mutations in the gene encoding copper-zinc superoxide dismutase (SOD1) causes approximately 20% cases of familial amyotrophic lateral sclerosis (FALS), characterized by selective loss of motor neurons. Mutant SOD1 forms inclusions in tissues from FALS patients. However, the precise mechanism of the accumulation of mutant SOD1 remains unclear. Here we show that human SOD1 is a substrate modified by SUMO-1. A conversion of lysine 75 to an arginine within a SUMO consensus sequence in SOD1 completely abolishes SOD1 sumoylation. We further show that SUMO-1 modification, on both wild type and mutant SOD1, increases SOD1 steady state level and aggregation. Moreover, SUMO-1 co-localizes onto the aggregates formed by SOD1. These findings imply that SUMO-1 modification on lysine 75 may participate in regulating SOD1 stability and its aggregation process. Thus, our results suggest that sumoylation of SOD1 may be involved in the pathogenesis of FALS associated with mutant SOD1.

关键词： FALS familial amyotrophic lateral sclerosis SOD1 copper-zinc superoxide dismutase sumoylation

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