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Contributions of NFKB1 -94insertion/deletion ATTG polymorphism to the susceptibility of gastrointestinal cancers: A meta-analysis.

ABSTRACT: Nuclear factor-kappa B1 (NF-κB1), a pleiotropic transcription factor, functions as a critical contributor to tumorigenesis. Growing numbers of case-control studies were carried out to analyse the potential contribution of NF-κB1 gene variants to gastrointestinal cancer risk, yet remains conflicting conclusions. Therefore, we conducted this most up-to-date meta-analysis to evaluate the relationship between NF-κB1 gene insertion (I)/deletion (D) polymorphism, namely -94ins/delATTG or rs28362491, and the susceptibility to gastrointestinal cancers. We searched PubMed, EMBASE and MEDLINE databases updated in April 2021 for relevant studies. Meta-analysis was carried out by software Stata11.0. The quantification of the relationship was determined by computing the combined odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Sensitivity analysis, the funnel plot and Begg's rank correlation test were also applied. Our findings indicate that -94ins/delATTG polymorphism could not significantly impact the susceptibility to gastrointestinal cancers. Under any five genetic models, -94ins/delATTG polymorphism was not remarkedly linked to the risk of colorectal, gastric and oesophageal cancer, respectively. The significant role of -94ins/delATTG was only observed in some certain subgroups. Findings here suggest that NF-κB1 gene -94ins/delATTG polymorphism may not predispose to gastrointestinal cancer susceptibility.

SUBMITTER: Wu H

PROVIDER: S-EPMC8581328 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Association between NFKB1 -94ins/del ATTG Promoter Polymorphism and Cancer Susceptibility: An Updated Meta-Analysis.

Project description:Nuclear factor- κ B is associated with the pathogenesis of numerous malignancies, and the functional polymorphism -94ins/del ATTG (rs28362491) in the human NFKB1 gene is associated with cancer risk. Previous studies on the association between the -94ins/del ATTG polymorphism and cancer risk reported conflicting results. To clarify this relationship, we performed a meta-analysis of 21 case-control studies involving 6127 cases and 9238 controls. We used pooled odds ratios (ORs) with their 95% confidence intervals (95% CIs) to assess the association. We found that the NFKB1 promoter -94ins/del ATTG polymorphism was significantly associated with cancer risk in four genetic models (ins/ins versus del/del, OR = 1.47, 95% CI = 1.11-1.93; dominant model, OR = 1.26, 95% CI = 1.03-1.53; recessive model, OR = 1.26, 95% CI = 1.05-1.51; ins allele versus del allele, OR = 1.19, 95% CI = 1.05-1.35). Stratified analyses revealed a significant association between the polymorphism and ovarian, oral, and prostate cancers. Similar results were determined in an Asian population and not in a Caucasian population. Thus, our results suggested that the polymorphism can contribute to cancer risk. Moreover, the polymorphism can exert race- and cancer-specific effects on cancer risk. Further large-scale and functional studies are necessary to elucidate this possible effect.

| S-EPMC4033547 | biostudies-literature

NFKB1 -94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies.

Project description:Nuclear factor-kappa B1 (NF-κB1) is a pleiotropic transcription factor and key contributor to tumorigenesis in many types of cancer. Numerous studies have addressed the association of a functional insertion (I)/deletion (D) polymorphism (-94ins/delATTG, rs28362491) in the promoter region of NFKB1 gene with the risk of various types of cancer; however, their conclusions have been inconsistent. We therefore conducted a meta-analysis to reevaluate this association. PubMed, EMBASE, China National Knowledge infrastructure (CNKI), and WANFANG databases were searched through July 2016 to retrieve relevant studies. After careful assessment, 50 case-control studies, comprising 18,299 cases and 23,484 controls were selected. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were used to determine the strength of the association. The NFKB1 -94ins/delATTG polymorphism was associated with a decreased risk of overall cancer in the homozygote model (DD vs. II): OR = 0.75, 95% CI = 0.64-0.87); heterozygote model (ID vs. II): OR = 0.91, 95% CI = 0.83-0.99; recessive model (DD vs. ID/II): OR = 0.81, 95% CI = 0.71-0.91; dominant model (ID/DD vs. II): OR = 0.86, 95% CI = 0.78-0.95; and allele contrast model (D vs. I): OR = 0.88, 95% CI = 0.81-0.95). Subgroup and stratified analyses revealed decreased risks for lung cancer, nasopharyngeal carcinoma, prostate cancer, ovarian cancer, and oral squamous cell carcinoma, and this association held true also for Asians (especially Chinese subjects) in hospital-based studies, and in studies with quality scores less than nine. Well-designed, large-scale case-control studies are needed to confirm these results.

| S-EPMC5354772 | biostudies-literature

An updated meta-analysis of 37 case-control studies on the association between NFKB1 -94ins/del ATTG promoter polymorphism and cancer susceptibility.

Project description: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.

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-94 ATTG insertion/deletion polymorphism of the NFKB1 gene is associated with coronary artery disease in Han and Uygur women in China.

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| S-EPMC3827022 | biostudies-literature

A functional NQO1 609C>T polymorphism and risk of gastrointestinal cancers: a meta-analysis.

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| S-EPMC3260285 | biostudies-literature

LAPTM4B polymorphism increases susceptibility to multiple cancers in Chinese populations: a meta-analysis.

Project description:BackgroundLysosome-associated protein transmembrane-4 beta (LAPTM4B) is a novel cancer-related gene. While recent studies have reported that the LAPTM4B polymorphism increased the susceptibility of several cancers, the results remain inconclusive. Therefore, we performed a meta-analysis to systematically summarize the possible association.ResultsThe meta-analysis was conducted based on 17 studies in Chinese populations, including 4160 cases and 4148 controls. The relevant studies were searched through electronic databases updated in November 2013. The strength of association between the LAPTM4B polymorphism and susceptibility to multiple cancers was assessed by odds ratio (OR) and 95% confidence interval (95% CI).The meta-analysis results suggested that the LAPTM4B polymorphism was significantly associated with overall susceptibility to multiple cancers in all genetic models (*2 vs. *1, OR = 1.53, 95% CI = 1.37-1.70; *2/2 vs. *1/1, OR = 2.18, 95% CI = 1.72-2.75; *2/1 vs.*1/1, OR = 1.62, 95% CI = 1.41-1.86; *2/1 + *2/2 vs. *1/1, OR = 1.70, 95% CI = 1.47-1.97; *2/2 vs. *2/1 + *1/1, OR = 1.76, 95% CI = 1.50-2.05). Further subgroup analysis revealed a significant association between the LAPTM4B polymorphism and cancer susceptibility in the subgroups stratified by control source, cancer type, histopathologic differentiation, and TNM stage.ConclusionsThis meta-analysis indicated that the LAPTM4B *2 allele was associated with increasing risk of multiple cancers, tumor initiation and development.

| S-EPMC4022328 | biostudies-literature

The association between NFKB1-94ins/del ATTG polymorphism and non-small cell lung cancer risk in a Chinese Han population.

Project description:This study aimed to clarify the influence of a common insertion/deletion polymorphism (-94ins/del ATTG, rs28362491) in the Nuclear factor-?B1 (NFKB1) promoter on non-small cell lung cancer (NSCLC) susceptibility. We genotyped the NFKB1 -94ins/del ATTG polymorphism by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and assessed the association with NSCLC risk, clinicopathological parameters in a case-control study of 421 cases and 425 controls. Heterozygous (ID) genotype disclosed a statistically significantly increased risk of developing NSCLC (OR = 1.57, 95% CI 1.13-2.19, P = 0.007). Homozygous (II) genotype also showed an increased risk of NSCLC (OR = 1.87, 95% CI 1.27-2.75, P = 0.001). Statistically significant difference was observed when the patients and controls were compared according to ID + II versus DD (OR = 2.01, 95% CI 1.47-2.76, P<0.001). The I allele was significantly higher in the NSCLC cases compared to the controls (52.9% versus 45.1%). The I allele was significantly associated with NSCLC risk (OR = 1.37, 95% CI 1.12-1.65, P = 0.001). There was a significantly higher frequency of ID + II genotypes observed in smokers, compared to non-smokers (OR = 1.99, 95% CI 1.22-3.24, P = 0.005) and in patients with stage III + IV, compared to stage I + II (OR = 2.16, 95% CI 1.34-3.49, P = 0.002). This study suggested that NFKB1 -94ins/del ATTG polymorphism was significantly associated with NSCLC risk in Chinese Han population.

| S-EPMC4509329 | biostudies-literature

Functional promoter -94 ins/del ATTG polymorphism in NFKB1 gene is associated with bladder cancer risk in a Chinese population.

Project description:BackgroundA functional -94 insertion/deletion polymorphism (rs28362491) in the promoter of the NFKB1 gene was reported to influence NFKB1 expression and confer susceptibility to different types of cancer. This study aims to determine whether the polymorphism is associated with risk of bladder cancer.Materials and methodsTaqMan assay was used to determine genotype among 609 cases and 640 controls in a Chinese population. Logistic regression was used to assess the association between the polymorphism and bladder cancer risk, and quantitative real-time polymerase chain reaction was used to determine NFKB1 mRNA expression.ResultsCompared with the ins/ins/ins/del genotypes, the del/del genotype was associated with a significantly increased risk of bladder cancer [adjusted odd ratio (OR) = 1.92, 95% confidence interval (CI) = 1.42-2.59]. The increased risk was more prominent among subjects over 65 years old (OR = 2.37, 95% CI= 1.52-3.70), male subjects (OR = 1.97, 95% CI = 1.40-2.79) and subjects with self-reported family history of cancer (OR = 3.59, 95% CI = 1.19-10.9). Furthermore, the polymorphism was associated with a higher risk of developing non-muscle invasive bladder cancer (OR= 2.07, 95% CI= 1.51-2.85), grade 1 bladder cancer (OR = 2.40, 95% CI = 1.68-3.43), single tumor bladder cancer (OR = 2.04, 95% CI = 1.48-2.82) and smaller tumor size bladder cancer (OR = 2.10, 95% CI= 1.51-2.92). The expression of NFKB1 mRNA in bladder cancer tissues with homozygous insertion genotype was higher than that with deletion allele.ConclusionsIn conclusion, the -94 ins/del ATTG polymorphism in NFKB1 promoter may contribute to the etiology of bladder cancer in the Chinese population.

| S-EPMC3748046 | biostudies-literature

Meta-analysis reveals a lack of association between UGT2B17 deletion polymorphism and tumor susceptibility.

Project description:PurposeUGT2B17 is a vital member of the UGT2 family and functions as a detoxification enzyme which catalyzes the glucuronidation of lipophilic compounds. Accumulating evidences implicates that it may contribute to the susceptibility of tumor risk. Identification of a UGT2B17 deletion polymorphism has attracted studies to evaluate the association between the UGT2B17 deletion polymorphism and tumor risk in diverse populations. However, the available results are conflicting.MethodsA meta-analysis based on 14 studies from 10 publications including 5,732 cases and 5,112 controls was performed. Published literature from PubMed, EMBASE and Web of Science was pooled and the crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the associations.ResultsConclusively, our results indicate that individuals with a UGT2B17 deletion polymorphism were associated with tumor risks (OR = 1.29, 95% CI = 1.03-1.63, P<0.001) in a recessive model. However, after excluding two studies for their heterogeneity, the result then demonstrated that the UGT2B17 deletion polymorphism was not associated with tumor risks (OR = 1.118, 95% CI = 0.938-1.332, P>0.1). A subgroup analysis based on tumor type, sex or race did not show significant results.ConclusionThese results suggest that the UGT2B17 deletion polymorphism is not associated with tumor risks.

| S-EPMC4011861 | biostudies-literature

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