Effects of FUS2 polymorphism on non-small cell lung cancer susceptibility and clinicopathological features

The FUS2 gene, residing in tumor suppressor gene region of human chromosome 3p21.3, has been considered as a promising tumor suppressor which may play critical roles in development of cancers. The present study was conducted to determine the effects of the FUS2 767A/T polymorphism on susceptibility and progression of NSCLC susceptibility in a Chinese population. The FUS2 767A/T polymorphism was genotyped in 252 NSCLC cases and 260 healthy controls using TaqMan method and DNA sequencing. Logistic regression was used to assess the genetic association between FUS2 767A/T polymorphism and occurrence and progression of NSCLC. The results revealed that subjects carrying T allele of the FUS2 767A/T polymorphism were at increased NSCLC risk as compared with the A allele carriers (T vs. A: adjusted OR=1.31, 95% CI=1.02-1.69, P=0.028). In addition, individuals carrying the AT genotype and at least 1 copy of T allele (dominant model) of the FUS2 767A/T polymorphism were confronted with increased NSCLC risk as compared with the wild-type AA genotype (AT vs. AA: adjusted OR=1.64, 95% CI=1.112.42, P=0.013; AT+TT vs. AA: adjusted OR=1.62, 95% CI=1.13-2.36, P=0.009). In subgroup analysis by smoking status, statistical significant increased NSCLC risk was observed among smokers. In association analysis between the FUS2 767A/T polymorphism and clinicopathological features of NSCLC, we found that patients carrying variant genotypes (AT+TT) had a significantly higher prevalence of advanced TNM stage, large tumor size, and positive lymph node metastasis. The results suggested that the functional FUS2 767A/T polymorphism may influence the susceptibility and progression of NSCLC in the Chinese population.