NFKB1 common variants and PPP1R13L and CD3EAP in relation to lung cancer risk in a Chinese population

• We evaluated NFKB1 5 htSNPs and gene–gene–environment interactions and lung cancer.
• No association was detected for individual htSNP in 4 genetic models.
• The haplotype consisting of 4 wild-type alleles was associated with lowered risk.
• Significant model of smoking duration–PPP1R13L rs1970764 interaction was tested.
• NFKB1 common variants and smoking–gene interaction could be concerned with the risk.

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 rs3774934G, rs13117745C, rs230541A, and rs1801G 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.