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)基因启动子区域甲摹化状态,分析GPX3甲基化与其基因表达的关系。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。
Objective 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-specifie 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 meehanism of its mRNA expression.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2012年第1期77-79,共3页
Chinese Journal of Experimental Surgery