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作 者:苗毅[1] 李保庆[1] 刘晖[2] 马玉泉[2] 贾涛[2] 田子强[1]
机构地区:[1]河北医科大学第四医院,河北石家庄056001 [2]邯郸市中心医院
出 处:《山东医药》2008年第38期17-20,共4页Shandong Medical Journal
基 金:国家自然科学基金资助项目(30400527);河北省科学技术研究与发展计划项目(08276101D-9)
摘 要:目的探讨金属硫蛋白3(MT-3)基因CpG岛超甲基化与食管鳞状细胞癌的关系。方法选取TE-1、TE-13、TTN和ECA-109四种食管鳞癌细胞株,用甲基化特异性聚合酶链反应和逆转录聚合酶链反应技术,在5-氮2′-脱氧胞苷(5-Aza-CdR)处理前后,对各细胞株的MT3基因CpG岛超甲基化及mRNA表达进行比较。结果四种食管鳞状细胞癌细胞株的MT3基因均存在不同程度的CpG岛超甲基化。5-aza-CdR处理后超甲基化状态解除,mRNA表达明显提高(P均<0.05)。结论食管鳞状细胞癌细胞株中MT3基因CpG岛超甲基化可抑制其mR-NA表达;超甲基化解除后MT3基因的mRNA表达相应升高。Objective To study the relationship between CpG island hypermethylation of MT3 gene and esophageal squamous cell carcinoma. Methods Four cell lines of squamous cell carcinoma of the esophagus TE-1, TE-13, TIN, ECA-109 were employed in this study. The comparison of CpG island hypermethylation status and the mRNA expression of MT3 gene of these four cell lines before and after treated by 5-Aza-2′-deoxycytidine(5-aza-CdR) was performed by using the techniques of methylation-specific PCR (MSP) and RT-PCR. Results Different degree of CpG island hypermethylation of MT3 gene existed in all the four cell lines of esophageal squamous cell carcinoma. The hypermethylation was demethylated after the treatment of 5-aza-CdR. CpG island hypermethylation mode was removed, the mRNA expression was also en- hanced obviously ( P 〈 0.05). Conclusions CpG island hypermethylation of MT3 gene in cell lines of esophageal squamous cell carcinoma can inhibit their mRNA expressions. When the hypermethylation is demethylated, the mRNA expression will be enhanced correspondly.
关 键 词:食管肿瘤 细胞株 金属硫蛋白3基因 甲基特异性聚合酶链反应 逆转录聚合酶链反应
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