前列腺癌细胞株E-钙粘连素基因启动子甲基化与其表达 |
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引用本文: | 李龙承,陈忠,张旭,叶章群,李家贵. 前列腺癌细胞株E-钙粘连素基因启动子甲基化与其表达[J]. 临床泌尿外科杂志, 2000, 15(11): 514-516 |
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作者姓名: | 李龙承 陈忠 张旭 叶章群 李家贵 |
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作者单位: | 同济医科大学附属同济医院泌尿外科武汉,430030 |
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摘 要: | 目的:了解E-钙粘连素(E-cad)基因启动子CpG位点甲基化与前殂腺癌细胞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mRNA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
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关 键 词: | E-钙粘连素 甲基化 前列腺癌 基因启动子 |
修稿时间: | 1999-09-23 |
A specific methylation pattern of the E-cadherin gene promoter is associated with its expression in prostate cancer lines |
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Abstract: | Objective: The present study was designed to test the hypothesis that CpG methylation ofpromoter region may inactivate the E-cadherin (E-cad)gene expression in prostate cancer line, and try tounderstand the mechanism of aberrant methylation. Methods:We studied the methylation status of E-cad gene inhuman prostate normal and cancer cell lines using the bisulfate genome sequencing technique. We also examinedthe 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-cadmRNA levels in these cell lines. Treatment with a demethylating agent, 5-aza-2′-deoxycytidine, restored E-cadmRNA levels in E-cad negative prostate cancer cell lines. Cancer cell lines had higher levels of Dnmtl mRNA thannormal cells. Conclusion:Our data clearly demonstrate that hypermethylation of E-cad in prostate cancer is acommon event that leads to the inactivation of the E-cad in prostate cancer is partly resulted by high level Dnmtl. |
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Keywords: | E-cadherin Methylation Prostate carcinoma |
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