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BioMed Research International
Volume 2015 (2015), Article ID 362542, 9 pages
http://dx.doi.org/10.1155/2015/362542
Research Article

Polymorphisms of NFκB1 and IκBα and Their Synergistic Effect on Nasopharyngeal Carcinoma Susceptibility

1The State Key Lab of Respiratory Disease, Collaborative Innovation Center for Environmental Toxicity, The Institute for Chemical Carcinogenesis, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou 510182, China
2Department of Genetics, Collaborative Innovation Center for Environmental Toxicity, Medical College of Soochow University, 199 Renai Road, Suzhou 215123, China

Received 5 June 2014; Revised 23 September 2014; Accepted 23 September 2014

Academic Editor: Yung-Fu Chang

Copyright © 2015 Yehua Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Nasopharyngeal carcinoma (NPC) is a multifactoral and polygenic disease with high prevalence in Southeast Asia and Southern China. Environmental factors and genetic susceptibility play important roles in NPC pathogenesis. In the present study, we tested the hypothesis that single nucleotide polymorphisms (SNPs) in nuclear factor-kappa B (NFκB) and its inhibitor (IκBα) conferred consistent risks for NPC. Four putatively functional SNPs (NFκB1: rs28362491del>ins ATTG; NFκB2: rs12769316G>A; IκBα: rs2233406C>T and rs696G>A) were analyzed to evaluate their associations with NPC risk in total 1590 NPC cases and 1979 cancer-free controls. We found that the rs28362491 insATTG variants (ins/del + ins/ins) in NFκB1 conferred an increased risk of NPC (odds ratio , 95% confidence interval –1.55, and ) compared with the del/del homozygous genotype. The rs696AA variant in IκBα had an increased risk of NPC (, 95% –1.66, and ) by decreasing IκBα expression due to the modulation of microRNA hsa-miR-449a. Furthermore, both adverse genotypes of NFκB/IκBα and their interaction also exerted an increased risk on NPC. Taken together, Our findings indicated that genetic variants in NFκB1 (rs28362491del>ins ATTG) and IκBα (rs696G>A) and their synergistic effect might contribute to NPC predisposition.