Genetic variations of TLR5 gene interacted with Helicobacter pylori infection among carcinogenesis of gastric cancer

// Tianwen Xu 1 , Deqiang Fu 1 , Yi Ren 2 , Yijun Dai 1 , Jianguang Lin 1 , Liming Tang 3 , Jian Ji 4 1 Department of Oncology, The Second Affiliated Hospital of Fujian Medical University, China 2 Department of Thyroid and Breast, Huai'an First People's Hospital, Nanjing Medical University, China 3 No. 2 People's Hospital of Henan Province, China 4 Department of Thoracic Surgery, Huai'an First People's Hospital, Nanjing Medical University, China Correspondence to: Jian Ji, email: jijian_huaian@sina.com Keywords: gastric cancer, variation, genetic, TLR5, helicobacter pylori Received: December 14, 2016 Accepted: January 11, 2017 Published: March 09, 2017 ABSTRACT Gastric cancer (GC) ranks the second prevalent cancer type and the second cancer-related death in China. However, the precise mechanisms of GC development remain poorly understood. Chronic infection with Helicobacter pylori is the strongest identified risk factor for GC. Toll-like receptor (TLR) genes, which play critical roles in Helicobacter pylori induced chronic inflammation, may also be implicated in GC susceptibility. TLR5 signaling deficiency could deregulate a cascade of inflammatory events. In current study, we systematically evaluated genetic variations of TLR5, and their interaction with Helicobacter pylori infection among carcinogenesis of gastric cancer, using a large case-controls study among Chinese population. Minor alleles of three SNPS, including rs5744174 ( P = 0.001), rs1640827 ( P = 0.005), and rs17163737 ( P = 0.004), were significantly associated with increased GC risk (OR ranged from 1.20–1.24). Significant interactions with Helicobacter pylori infection were also identified for rs1640827 (P for interaction = 0.009) and rs17163737 (P for interaction = 0.006). These findings suggest that genetic variants in TLR5 may modify the role of Helicobacter pylori infection in the process of causing GC.