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作 者:李龙承[1] 陈忠[1] 张旭[1] 叶章群[1] 李家贵[1]
机构地区:[1]同济医科大学附属同济医院泌尿外科,武汉430030
出 处:《临床泌尿外科杂志》2000年第11期514-516,共3页Journal of Clinical Urology
摘 要:目的 :了解 E-钙粘连素 (E- cad)基因启动子 Cp G位点甲基化与前列腺癌细胞 E- cad基因的失活的关系 ,并探讨 E- cad基因异常甲基化机制。方法 :采用硫酸氢钠基因组测序法检测良性前列腺上皮和前列腺癌细胞株的 E- cad基因甲基化状态 ,并采用 RT- PCR检测各细胞株 E- cad和 DNA甲基转移酶 (Dnmtl)的 m RNA表达。结果 :有 33% (2 /6)的前列腺癌细胞株发生甲基化现象 ,相应的细胞株中 E- cad m RNA水平降低。用去甲基化剂偶氮胞嘧啶 (Aza C)处理后 ,能恢复 E-cad阴性的前列腺癌细胞株中 E- cad m RNA水平。前列腺癌细胞株比正常上皮细胞株有较高水平的 Dnmtl表达。结论 :前列腺癌细胞 E- cad基因的高甲基化状态是引起该基因失活的原因 ,基因的异常甲基化可能与 Dnmtl有关。Objective:The present study was designed to test the hypothesis that CpG methylation of promoter region may inactivate the E-cadherin(E-cad)gene expression in prostate cancer line,and try to understand the mechanism of aberrant methylation.Methods:We studied the methylation status of E-cad gene in human prostate normal and cancer cell lines using the bisulfate genome sequencing technique.we also examined the expression of the E-cad gene and DNA methyltransferase(Dnmtl)in these lines by RT-PCR.Results:Hypermethylation was found in 33% of prostate cancer cell lines(2/6)and correlated well with decreased E-cad mRNA levels in these cell lines.Treatment with a demethylating agent,5-aza-2′-deoxycytidine,restored E-cad mRNA levels in E-cad negative prostate cancer cell lines.Cancer cell lines had higher levels of Dnmtl mRNA than normal cells.Conclusion:Our data clearly demonstrate that hypermethylation of E-cad in prostate cancer is a common event that leads to the inactivation of the E-cad in prostate cancer is partly resulted by high level Dnmtl.
分 类 号:R737.250.2[医药卫生—肿瘤]
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