Association Between the <i>XRCC6</i> Promoter <i>rs2267437</i> Polymorphism and Cancer Risk: Evidence Based on the Current Literature

Hui, Xu; Zou, Peng; Chen, Pin; Zhao, Lin; Zhao, Peng; Lü, Aiping

doi:10.1089/gtmb.2013.0083

Cited by 7 publications

(8 citation statements)

References 35 publications

(38 reference statements)

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“…A number of polymorphisms have been identified in the XRCC6 promoter that correlate with increased carcinogenesis. The Ku70 C-61G polymorphism (SNP rs2267437) is associated with increased breast cancer incidence, RCC, HCC, prostate, and lung cancer [ 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 ]. The Ku70 promoter T-991C (SNP rs5751129) polymorphism is associated with HCC, gastric, oral, renal, and nasopharyngeal cancer susceptibility, and this novel polymorphism is predicted to lead to differential XRCC6 mRNA and Ku70 protein expression levels [ 115 , 120 , 121 , 122 , 123 ].…”

Section: Core Nhej Factors In Carcinogenesis and Cancermentioning

confidence: 99%

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

Sishc

Davis

2017

Cancers

135

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DNA double-strand breaks (DSBs) are deleterious DNA lesions that if left unrepaired or are misrepaired, potentially result in chromosomal aberrations, known drivers of carcinogenesis. Pathways that direct the repair of DSBs are traditionally believed to be guardians of the genome as they protect cells from genomic instability. The prominent DSB repair pathway in human cells is the non-homologous end joining (NHEJ) pathway, which mediates template-independent re-ligation of the broken DNA molecule and is active in all phases of the cell cycle. Its role as a guardian of the genome is supported by the fact that defects in NHEJ lead to increased sensitivity to agents that induce DSBs and an increased frequency of chromosomal aberrations. Conversely, evidence from tumors and tumor cell lines has emerged that NHEJ also promotes chromosomal aberrations and genomic instability, particularly in cells that have a defect in one of the other DSB repair pathways. Collectively, the data present a conundrum: how can a single pathway both suppress and promote carcinogenesis? In this review, we will examine NHEJ’s role as both a guardian and a disruptor of the genome and explain how underlying genetic context not only dictates whether NHEJ promotes or suppresses carcinogenesis, but also how it alters the response of tumors to conventional therapeutics.

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Section: Core Nhej Factors In Carcinogenesis and Cancermentioning

confidence: 99%

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

Sishc

Davis

2017

Cancers

135

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“…Until recently, the meta-analyzes assessing the association between XRCC6 polymorphisms and cancer 17 – 19 are limited to one single polymorphism site. Systematic review of association between XRCC6 polymorphisms and cancer risk is lacking, and the role of XRCC6 in the etiology of cancer is still equivocal.…”

Section: Introductionmentioning

confidence: 99%

Association Between the XRCC6 Polymorphisms and Cancer Risks

et al. 2015

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A number of studies have been carried out to investigate the association of X-ray repair complementing defective repair in Chinese hamster cells 6 (XRCC6) polymorphisms and cancer risks, and the results remained inconsistent and inconclusive.To assess the effect of XRCC6 polymorphisms on cancer susceptibility, we conducted a meta-analysis, up to May 23rd 2014, 6267 cases with different types of tumor and 7536 controls from 20 published case–control studies. Summary odds ratios and corresponding 95% confidence intervals for XRCC6 polymorphism and cancer risk were estimated using fixed- or random-effects models when appropriate. Heterogeneity was assessed by chi-squared-based Q-statistic test, and the sources of heterogeneity were explored by subgroup analyses, logistic meta-regression analyses and Galbraith plot. Publication bias was evaluated by Begg funnel plot and Egger test. Sensitivity analyses were also performed.The rs2267437 polymorphism was associated with a significant increase in risks of overall cancers, breast cancer, renal cell carcinoma and hepatocellular carcinoma, and it could increase the cancer risk in Asian population; the rs5751129 polymorphism could increase the cancer risk in overall cancers; the rs132770 polymorphism was associated with the increased renal cell carcinoma risk; furthermore, the rs132793 polymorphism could decrease breast cancer risk and increase risks in “other cancers”.Overall, the results provided evidences that the single nucleotide polymorphisms in XRCC6 promoter region might play different roles in various cancers, indicating different cancers have different tumorigenesis mechanisms. Our studies may perhaps supplement for the disease monitoring of cancers in the future, and additional studies to determine the exact molecular mechanism might provide us with interventions to protect the susceptible subgroups.

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“…The polymorphisms in these genes and the susceptibility to various cancers such as breast , hepatocellular and digestive system cancer have been reported. Human XRCC6 maps to chromosome 22 and specifically the rs2267437 polymorphism (C > G) is located in the promoter of the gene . Studies have investigated the association between this polymorphism and cancer susceptibility.…”

mentioning

confidence: 99%

“…Studies have investigated the association between this polymorphism and cancer susceptibility. The results of these studies have been controversial, but investigations suggest that the rs2267437 polymorphism may affect breast cancer susceptibility in Asian populations . To date, there are a limited amount of studies available regarding the effects of the XRCC6 polymorphism rs2267437 upon CRC risk.…”

mentioning

confidence: 99%

Gene polymorphism in DNA repair genes XRCC1 and XRCC6 and association with colorectal cancer in Swedish patients

Dimberg

Skarstedt

Olsen

et al. 2016

APMIS

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The DNA repair genes XRCC1 and XRCC6 have been proposed to participate in the pathological process of cancer by modulating the DNA repair capacity. This study evaluated the susceptibility of the single-nucleotide polymorphisms (SNPs) XRCC1 (rs25487, G > A) and XRCC6 (rs2267437, C > G) to colorectal cancer (CRC) and their association with clinical parameters in Swedish patients with CRC. Using the TaqMan system, these SNPs were screened in 452 patients and 464 controls. No significant difference in genotype distribution was found between the patients and controls, or any significant association with cancer-specific or disease-free survival in patients. However, we showed that the carriers of allele A in XRCC1 (rs25487, G > A) were connected with a higher risk of disseminated CRC (Odds Ratio = 1.64; 95% Confidence Interval = 1.12-2.41, p = 0.012).

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Association Between the XRCC6 Promoter rs2267437 Polymorphism and Cancer Risk: Evidence Based on the Current Literature

Cited by 7 publications

References 35 publications

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

Association Between the XRCC6 Polymorphisms and Cancer Risks

Gene polymorphism in DNA repair genes XRCC1 and XRCC6 and association with colorectal cancer in Swedish patients

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