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首页> 外文期刊>Molecular Carcinogenesis >Association of a functional RAD52 genetic variant locating in a miRNA binding site with risk of HBV-related hepatocellular carcinoma
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Association of a functional RAD52 genetic variant locating in a miRNA binding site with risk of HBV-related hepatocellular carcinoma

机译：定位在miRNA结合位点的功能性RAD52遗传变异与HBV相关肝细胞癌的风险相关

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As an important member in homologous recombination repair, RAD52 plays a crucial part in maintaining genomic stability and prevent carcinogenesis. Several cancer susceptibility RAD52 single nucleotide polymorphisms (SNPs) have been identified previously. However, little or nothing has been known about the RAD52 SNPs and their functional significance in hepatitis B viruses (HBV)-related hepatocellular carcinoma (HCC). Therefore, we investigated the association between five RAD52 SNPs (rs1051669, rs10774474, rs11571378, rs7963551, and rs6489769) and HBV-related HCC risk as well as its biological function in vivo. Genotypes were determined in two independent case-control sets from two regions of China. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression. The allele-specific regulation on RAD52 expression by the functional genetic variant was examined with normal liver tissues. We found that only the RAD52 rs7963551 SNP was significantly associated with HCC risk, with the odds of having the rs7963551 CC genotype in patients was 0.59 (95% CI=0.45-0.78, P=1.5x10(-4), HCC cases versus chronic HBV carriers) or 0.65 (95% CI=0.52-0.81, P=1.1x10(-4), HCC cases versus healthy controls) compared with the AA genotype. In the genotype-phenotype correlation analyses of 44 human liver tissue samples, rs7963551 CC or AC was associated with a statistically significant increase of RAD52 mRNA expression, which are consistent to functional relevance of allelic regulation of RAD52 expression by rs7963551 SNP and miRNA let-7 in cancer cells. Our data demonstrated that RAD52 functional rs7963551 SNP contributes to susceptibility to developing HCC. (c) 2014 Wiley Periodicals, Inc.
机译：作为同源重组修复的重要成员，RAD52在维持基因组稳定性和预防癌变中起着至关重要的作用。先前已经确定了几种癌症易感性RAD52单核苷酸多态性（SNP）。但是，关于RAD52 SNP及其在乙型肝炎病毒（HBV）相关的肝细胞癌（HCC）中的功能意义了解甚少，甚至一无所知。因此，我们研究了五个RAD52 SNP（rs1051669，rs10774474，rs11571378，rs7963551和rs6489769）与HBV相关的HCC风险及其在体内的生物学功能之间的关联。在来自中国两个地区的两个独立的病例对照集中确定了基因型。通过逻辑回归估计赔率（OR）和95％置信区间（CI）。用正常肝组织检查功能基因变异对RAD52表达的等位基因特异性调控。我们发现只有RAD52 rs7963551 SNP与HCC风险显着相关，患者拥有rs7963551 CC基因型的几率是0.59（95％CI = 0.45-0.78，P = 1.5x10（-4），HCC患者与慢性与AA基因型相比，HBV携带者）或0.65（95％CI = 0.52-0.81，P = 1.1x10（-4），HCC病例与健康对照）。在44个人类肝脏组织样本的基因型与表型相关性分析中，rs7963551 CC或AC与RAD52 mRNA表达的统计学显着增加相关，这与rs7963551 SNP和miRNA let-7等位基因调控RAD52表达的功能相关性相一致。在癌细胞中。我们的数据表明，RAD52功能性rs7963551 SNP有助于发展HCC。 （c）2014年威利期刊有限公司

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