Abstract
As a cell survival signal, nuclear factor-kappa B (NFKB) is associated with the pathogenesis of numerous malignancies. According to several studies, NFKB1 −94ins/del ATTG promoter polymorphism is associated with the risk of different malignancies, but the results were not consistent. Therefore, we performed an updated meta-analysis based on 37 case-control studies from 33 articles (16,271 cases and 22,781 controls) to clarify the relationship. The odds ratio (OR) and 95% confidence interval (CI) were used to determine the strength of the association. We found that the NFKB1 −94ins/del ATTG promoter polymorphism was significantly associated with increased susceptibility to cancer in the recessive (II vs. ID+DD, OR = 1.140, 95% CI = 1.029–1.263, p =0.012), homozygote (II vs. DD, OR = 1.259, 95% CI = 1.068–1.485, p =0.006), and allele (I vs. D, OR = 1.109, 95% CI = 1.025–1.199, p =0.010) genetic models. The subgroup analysis for ethnicity found that the NFKB1 −94ins/del ATTG promoter polymorphism was significantly associated with an increased susceptibility to cancer in Asians and with a decreased susceptibility in Caucasians. The stratified analyses revealed significant associations between the polymorphism and increased susceptibility to ovarian cancer, oral squamous cell carcinoma, and nasopharyngeal carcinoma.
Highlights
Cancer is the result of complex interactions between inherited and environmental factors, which threatens people worldwide due to high morbidity and mortality [1]
We found that the NFKB1 -94ins/del ATTG promoter polymorphism was significantly increased cancer risk in homozygote (II vs. DD, odds ratio (OR) = 1.259, 95% confidence interval (CI) = 1.068-1.485), recessive (II vs. ID+DD, OR = 1.140, 95% CI = 1.029-1.263) and allele (I vs. D, OR = 1.109, 95% CI = 1.025-1.199) genetic models
We found that the NFKB1 -94ins/del ATTG promoter polymorphism was significantly associated with increased risk of cancer; this result was different than a previous meta-analysis [48], which reported that there was no association between the NFKB1 -94ins/del ATTG promoter polymorphism and cancer risk
Summary
Cancer is the result of complex interactions between inherited and environmental factors, which threatens people worldwide due to high morbidity and mortality [1]. The aetiology of this disease remains unclear, genetic susceptibility is one known explanation for the inter-individual variation in cancer risk [2]. Many researchers have been studying the aetiology of oncogenesis, and have identified the relationship between genetic polymorphism and cancer risk, especially for the NFKB1 -94ins/del ATTG promoter polymorphism. NFKB is responsible for regulating the expression of many genes for immune response, cell adhesion, differentiation, proliferation, angiogenesis and apoptosis [3]. NFKB binds to a 10 bp DNA element in kappa immunoglobulin light-chain enhancer in B cells [5]. The human NFKB1 gene, located on chromosome 4q24, encodes a 50 kDa DNA-binding protein that can act as a master regulator of inflammation and cancer development [6,7]
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