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锰超氧化物歧化酶9AlaVal、抵抗素基因启动子-420CG单核苷酸多态性与吸烟的交互作用和食管鳞状细胞癌的关系
Interaction of single nucleotide polymorphisms of manganese superoxide dismutase9Ala/Val, resistin gene promoter -420C/G and cigarette smoking in esophageal squamous cell carcinoma

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DOI:
作者:
张超贤
ZHANG Chaoxian
作者单位:
新乡医学院第一附属医院
The First Affiliated Hospital of Xinxiang Medical University
关键词:
食管鳞状细胞癌(ESCC)；锰超氧化物歧化酶9Ala/Val(MnSOD9Ala/Val)；抵抗素基因启动子-420C/G；多态现象；吸烟
esophageal squamous cell carcinoma(ESCC); manganese superoxide dismutase9Ala/Val(MnSOD9Ala/Val); resistin gene promoter -420C/G; polymorphism; cigarette smoking
摘要:
【摘要】 目的 探讨锰超氧化物歧化酶9Ala/Val(manganese superoxide dismutase9Ala/Val, MnSOD9Ala/Val)、抵抗素基因启动子-420C/G单核苷酸多态性与吸烟的交互作用和食管鳞状细胞癌(esophageal squamous cell carcinoma, ESCC)的关系。方法 采用病例-对照研究的方法，以720例ESCC患者及720例健康对照者的外周血白细胞为样本，利用聚合酶链反应(polymerase chain reaction, PCR)技术分析了MnSOD9Ala/Va和抵抗素基因启动子-420C/G多态性。结果 MnSOD9Ala/Val (VV)基因型和-420C/G(GG)基因型频率分布分别为50.14%、49.86% (病例组)和24.17%、23.89% (对照组)，二者经χ2 检验差异有显著性(P<0.01；P<0.01)。MnSOD9Ala/Val (VV)基因型患ESCC的风险显著增加(OR=3.1553，95%CI= 1.8062-5.1451 )。-420C/G(GG)基因型者患ESCC的风险也显著增加(OR= 3.1683，95%CI= 1.9254-5.2062 )。基因突变的协同分析发现MnSOD9Ala/Val (VV)/ -420C/G(GG)基因型者在ESCC组和对照组中的分布频率分别为39.72%和12.78%，二者经χ2检验有显著性差异(P<0.01)。MnSOD9Ala/Val (VV)/ -420C/G(GG)基因型者患ESCC的风险显著增加(OR=5.0651，95%CI=3.1879-7.8481)。病例组的吸烟率显著高于对照组的吸烟率（OR= 3.3264，95%CI= 1.9075-5.7406，P<0.01)，吸烟与MnSOD9Ala/Val (VV)和-420C/G(GG)基因型与均有交互作用(γ=3.9266；γ=3.9383)。结论MnSOD9Ala/Val (VV)、-420C/G(GG)基因型和吸烟是ESCC的易患因素，基因多态性与吸烟的交互作用增加了ESCC的发病风险。
【Abstract】Objective To investigate the interaction between single nucleotide polymorphisms of manganese superoxide dismutase9Ala/Val(MnSOD9Ala/Val), resistin gene promoter -420C/G and cigarette smoking in esophageal squamous cell carcinoma(ESCC). Methods The genetic polymorphisms of MnSOD9Ala/Val and resistin gene promoter -420C/G were analyzed by polymorphism-polymerase chain reaction (PCR) technique in peripheral blood leukocytes of 720 ESCC cases and 720 healthy persons. Results The frequencies of MnSOD9Ala/Val (VV) and -420C/G(GG) were 50.14% and 49.86% in ESCC cases and 24.17% and 23.89% in healthy controls respectively. Statistical tests showed significant difference in the frequencies between the two groups (P<0.01) . The risk of ESCC with MnSOD9Ala/Val (VV) was significantly higher than those of controls (OR=3.1553, 95%CI= 1.8062-5.1451). The individuals who carried with -420C/G (GG) had a high risk of ESCC (OR= 3.1683, 95%CI= 1.9254-5.2062). Combined analysis of the polymorphisms showed that percentage of MnSOD9Ala/Val (VV) / -420C/G(GG) in ESCC and control groups was 39.72% and 12.78% respectively( P<0.01). The people who carried with MnSOD9Ala/Val (VV) / -420C/G(GG) had a high risk of ESCC (OR=5.0651, 95%CI= 3.1879-7.8481).The cigarette smoking rate of the case group was significantly higher than which in the control group (OR= 3.3264, 95%CI= 1.9075-5.7406, P<0.01) ,and statistic analysis suggested an interaction between cigarette smoking and MnSOD9Ala/Val (VV) and -420C/G(GG) which increase risk of ESCC (γ=3.9266; γ=3.9383). Conclusion MnSOD9Ala/Val (VV), -420C/G(GG) and cigarette smoking are the risk factors in ESCC, and the significant interactions between geneticpolymorphisms of MnSOD9Ala/Val (VV), -420C/G(GG) and cigarette smoking added the risk of ESCC.

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