Effects of NAT2 Polymorphism on Lung Cancer Risk, and the Interaction Between Smoking and NAT2: A Meta-analysis

Abstract

Background Lung cancer is the most common cancer in the world, and cancer death is mainly caused by lung cancer. At present, the etiology and pathogenesis of lung cancer are not clear. N-acetyltransferase 2 (NAT2) is an enzyme found in the lungs, colon, breast, prostate, and liver. NAT2 is polymorphic and can metabolize carcinogens from tobacco smoke. At present, many studies have explored the effects of NAT2 polymorphism on lung cancer, but we found inconsistent results. Methods We conducted a research of 19 published studies, involving 4,130 patients and 6,057 controls, to more accurately assess the effects of NAT2 polymorphism on lung cancer risk and to investigate whether smoking is associated. We used STATA software to analyze the extracted data and used STATA for subgroup analysis, sensitivity analysis, and to perform publication bias tests. To determine the correlation, we used the crude odds ratio (ORs) with 95% confidence interval (CIs). Results From the major results, we found that there was no significant correlation between NAT2 polymorphism and lung cancer (OR = 1.00, 95% CI: 0.84–1.19, I² = 63.3%, P < 0.001 for heterogeneity). We also found no significant results in stratified analyses of smoking, ethnicity, gender, and source of controls. However, we learned from the subgroup analysis that the lung cancer risk in NAT2 patients with intermediate-slow acetylation may be increased (OR = 1.83, 95% CI: 1.22–2.73, I² = 39.6%, P = 0.191 for heterogeneity). Conclusions This research showed that no sufficient evidence was found to prove the effect of NAT2 polymorphism on lung cancer risk; however the increased acetylation capacity of NAT2 might reduce the risk of lung cancer.