Yin Jiaoyang, Yin Mengfan, Vogel Ulla, Wu Yuhong, Yao Tao, Cheng Yanhua, Sun Zhenxiang, Hou Wei, Wang Chunhong
Key Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang 110034, Liaoning Province, People's Republic of China.
Department of orthopedics, Tianjin Fifth Center Hospital, Tianjin 300450, People's Republic of China.
Gene. 2015 Aug 1;567(1):31-5. doi: 10.1016/j.gene.2015.04.059. Epub 2015 Apr 23.
Genetic variations in NFKB1 have been associated with cancer risk. This investigation intended to evaluate the possible association between common variants in NFKB1 and lung cancer risk and gene-gene and gene-environment interactions. A study containing 384 Chinese lung cancer cases and 387 cancer-free controls was conducted. 5 htSNPs (rs3774934, rs13117745, rs230541, rs1801, rs3774965) in NFKB1 and interaction with common variants in NFKB1 and PPP1R13L and CD3EAP and smoking-duration were assessed. No association with lung cancer risk was detected for individual htSNP in four genetic models, but the haplotype consisting of the wild-type alleles of rs3774934(G), rs13117745(C), rs230541(A), and rs1801(G) was associated with lowered lung cancer risk after adjustment for smoking duration [OR (95% CI) = 0.71 (0.51-0.98), P = 0.036]. There was no interaction between NFKB1 polymorphisms and PPP1R13L and CD3EAP and smoking status in relation to lung cancer risk. Two significant models: smoking duration as main effect (P < 0.0010) and smoking duration-PPP1R13L rs1970764 combination (P = 0.0040-0.0050) were tested. The results suggest that NFKB1 common variants and smoking duration and smoking duration-PPP1R13L rs1970764 interaction could be concerned with the lung cancer development in a Chinese population. The present findings add to the evidence implicating inflammation in lung cancer etiology.
NFKB1基因的遗传变异与癌症风险相关。本研究旨在评估NFKB1常见变异与肺癌风险以及基因-基因和基因-环境相互作用之间的可能关联。开展了一项包含384例中国肺癌病例和387例无癌对照的研究。评估了NFKB1中的5个单倍型特异性单核苷酸多态性(htSNP,rs3774934、rs13117745、rs230541、rs1801、rs3774965)以及NFKB1与PPP1R13L和CD3EAP常见变异和吸烟持续时间的相互作用。在四种遗传模型中,未检测到单个htSNP与肺癌风险的关联,但在调整吸烟持续时间后,由rs3774934(G)、rs13117745(C)、rs230541(A)和rs1801(G)的野生型等位基因组成的单倍型与肺癌风险降低相关[比值比(95%可信区间)=0.71(0.51-0.98),P=0.036]。NFKB1多态性与PPP1R13L和CD3EAP以及吸烟状态在肺癌风险方面不存在相互作用。测试了两个显著模型:以吸烟持续时间为主要效应(P<0.0010)和吸烟持续时间-PPP1R13L rs1970764组合(P=0.0040-0.0050)。结果表明,NFKB1常见变异、吸烟持续时间以及吸烟持续时间-PPP1R13L rs1970764相互作用可能与中国人群的肺癌发生有关。目前的研究结果进一步证明炎症与肺癌病因有关。