乳头状甲状腺癌中谷胱甘肽过氧化物酶3启动子区高甲基化与表达缺失
Glutathione peroxidase 3 promoter region hypermethylation and loss of expression in papillary thyroid carcinomas
摘要目的 探讨乳头状甲状腺癌(PTC)中谷胱甘肽过氧化物酶3(GPX3)基因启动子区域甲基化状态,分析GPX3甲基化与其基凶表达的关系.方法 应用甲基化特异性聚合酶链式反应(MSP)检测47例PTC、10例非癌组织标本和乳头状甲状腺癌细胞株TPC-1中GPX3的甲基化状态,并用逆转录-聚合酶链式反应(RT-PCR)检测TPC-1细胞中GPX3的mRNA表达.结果 48.9%( 23/47) PTC发生GPX3基因启动子区域甲基化,而10例非癌组织均未发生甲基化;TPC-1中GPX3启动子区甲基化,而且GPX3的mRNA不表达,经5-aza-2’-deoxycytidine干预96h后GPX3重新表达.结论 GPX3基因启动子区域频繁发生甲基化.,可能作为PTC的诊断标志物;GPX3启动子区的甲基化是其基因表达的重要调节机制.
更多相关知识
abstractsObjective To explore the station of glutathione peroxidase 3 (GPX3) promoter region methylation in papillary thyroid carcinoma (PTC) and analyze the relationship between the expression of GPX3 and its methylation.Methods Methylation-specific polymerase chain reaction (MSP) was employed to detect GPX3 gene promoter region methylation in 47 papillary thyroid carcinoma samples,10 non-cancerous tissues and the papillary thyroid carcinoma cell line TPC-1.By using reverse transcription polymerase chain reaction (RT-PCR) the mRNA expression of GPX3 wad detected in TPC-1 cells.Results 48.9% (23/47) of PTC was methylated,while none of the 10 non-cancerous tissues was methylated.The promoter of GPX3 was hypermethylated in TPC-1 cells,and after treatment of TPC-1 with 5-aza-2' -deoxycytidine for 96 h,the mRNA of GPX3 was re-expressed.Conclusion GPX3 promoter region methylation probably become PTC diagnostic marker.GPX3 promoter hypermethylation is an important epigenetic regulation mechanism of its mRNA expression.
More相关知识
- 浏览456
- 被引18
- 下载132

相似文献
- 中文期刊
- 外文期刊
- 学位论文
- 会议论文