| 非同源末端连接修复通路DNA-PKcs基因在胶质瘤中表达及其机制研究 |
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| 引用本文： | 庄志祥,沈丽琴,张舒羽,邱鹏. 非同源末端连接修复通路DNA-PKcs基因在胶质瘤中表达及其机制研究[J]. 中国肿瘤临床, 2010, 37(4): 216-219. DOI: 10.3969/j.issn.1000-8179.2010.04.011 |
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| 作者姓名： | 庄志祥 沈丽琴 张舒羽 邱鹏 |
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| 作者单位： | 苏州大学附属第二医院肿瘤科(苏州市215004);①复旦大学遗传学研究所 |
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| 摘 要： | 目的:研究DNA双链断裂损伤修复通路主要成员Ku70、Ku80、ERCC4、Lig4 和DNA-PKcs 基因在人脑胶质瘤中的mRNA 表达及其与肿瘤发生的关系。方法:采用SYBR Green实时定量PCR 技术检测36例人原发脑胶质瘤组织和12例正常脑组织中的Ku70、Ku80、ERCC4、Lig4 和DNA-PKcs 的mRNA 水平。用亚硫酸盐处理基因组DNA后，采用甲基化特异的聚合酶链式反应（MSP）检测正常脑组织和胶质瘤组织中DNA-PKcs 基因的甲基化水平变化。结果:与正常脑组织相比，Ku70、Ku80、ERCC4、Lig4 基因表达量在脑胶质瘤和正常脑组织中无显著性变化（P>0.05），DNA-PKcs 基因在脑胶质瘤中表达显性著上调（P=0.002）。DNA-PKcs 基因在脑胶质瘤组织中表达量随胶质瘤恶性程度升高而增加。DNA-PKcs 基因启动子甲基化程度在正常组织中高于肿瘤组织，表明甲基化程度的减少是引起胶质瘤中DNA-PKcs 基因表达增高的原因。结论:DNA-PKcs 基因在人脑胶质瘤中较正常脑组织表达显著上调，并且表达与脑胶质瘤的恶性程度相关。DNA-PKcs 基因甲基化程度的降低是引起胶质瘤中DNA-PKcs基因表达增高的原因。
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| 关 键 词： | 脑胶质瘤 非同源末端连接修复 DNA-PKcs 基因 甲基化 实时荧光定量PCR |
| 收稿时间： | 2009-10-26 |
Up-regulation of DNA-PKcs and Its Mechanism in Human Glioma |
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| ZHUANG Zhixiang,SHEN Liqin,ZHANG Shuyu,QIU Peng. Up-regulation of DNA-PKcs and Its Mechanism in Human Glioma[J]. Chinese Journal of Clinical Oncology, 2010, 37(4): 216-219. DOI: 10.3969/j.issn.1000-8179.2010.04.011 |
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| Authors: | ZHUANG Zhixiang SHEN Liqin ZHANG Shuyu QIU Peng |
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| Affiliation: | 1Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China |
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| Abstract: | Objective: To detect the gene expression of Ku70, Ku80, ERCC4, lig4 and DNA-PKcs in non-homologous end joining pathway in human pdmary glioma tissues and normal brain tissues and to explore the underlying mechanism. Methods: The expression levels of Ku70, Ku80, ERCC4, lig4 and DNA-PKcsin in 36 glioma samples and 12 normal brain tissue samples were measured by SYBR Green real-time quantitative PCR. Methylation of DNA-PKcs was detected by methylation-specific PCR (MSP). Results: There was no significant difference in Ku70, Ku80, ERCC4 and lig4 expression between human primary glioma and normal brain tissues (P<0.05), while DNA-PKcs was significantly up-regulated (P= 0.002). The expression of DNA-PKcs was significantly higher in grade Ⅲ and Ⅳ glioma than that in grade Ⅱ glioma and normal brain tissues (P<0.05). Moreover, glioma tissues showed weaker methylation than normal brain tissues. Conclusion: The up-regulation of DNA-PKcs may be associated with pathogenesis of glioma. Demethylation of DNA-PKcs promoter is an important reason for its up-regulated expression in glioma. |
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| Keywords: | Glioma Non-homologous end joining DNA-PKcs Methylation Real-time PCR |
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