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前列腺癌中EphA1基因表达的初步研究 被引量:4

EphA1 expression and prostate cancer
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摘要 目的:检测前列腺癌中EphA1基因转录及受体表达水平,探讨其表达异常的机制及其临床意义。方法:利用RT-PCR法检测雄激素依赖性前列腺癌细胞系LNCaP和雄激素非依赖性前列腺癌细胞系PC-3中EphA1基因mRNA表达情况,采用甲基化特异性PCR(MSP)方法进行甲基化状态分析;用免疫组化方法检测19例前列腺癌和22例良性前列腺组织标本中EphA1受体表达情况。结果:LNCaP和PC-3细胞中均未检测到EphA1基因转录;PC-3细胞中EphA1基因启动子区内CpG岛存在高甲基化现象,而LNCaP细胞则不存在;前列腺癌和良性前列腺增生组织中EphA1受体表达率分别为36.8%和45.5%,其差异无统计学意义(P>0.05)。结论:前列腺癌细胞LNCaP和PC-3中无明显EphA1基因表达,甲基化可能是导致该基因下调的机制之一。EphA1基因的甲基化在前列腺癌进展及由雄激素依赖向雄激素非依赖转化过程中可能发挥一定作用。 Objective: To examine the expression of the EphA1 gene in prostate cancer and to determine the mechanism underlying the aberrance of the expression and its clinical significance. Methods: The expressions of the EphA1 gene in prostate cancer cell lines LNCaP (androgen-sensitive) and PC-3 (androgen-insensitive) were detected by RT-PCR, and the methylation status of the CpG island of the EphA1 promoter analyzed with methylation specific PCR (MSP). The expressions of the EphA1 receptor in 19 prostate cancer and 22 BPH tissue samples were determined by immunohistochemical staining. Results: The expression of EphA1 mRNA was not observed in LNCaP and PC-3 cells. Hypermethylation of the CpG island of EphA1 was found in PC-3 but not LNCaP cells. The expression rates of the EphA1 receptor were 36.8% (7/19) and 45.5% (10/22) respectively in the prostate cancer and the BPH specimens, with no statistical significant difference in between (P 〉0. 05 ). Conclusion:There is no detectable expression of theEphA1 gene in prostate cancer cell lines PC-3 and LNCaP; hypermethylation of the CpG island may be one of the mechanisms underlying the down-regulation of the expression. EphA1 methylation might play a role in the progression of prostate cancer and its transformation from androgen-dependence to androgen-independence.
出处 《医学研究生学报》 CAS 2008年第5期451-454,I0001,共5页 Journal of Medical Postgraduates
基金 国家杰出青年基金资助项目(批准号:30225046) 南京军区科学技术“十一五”计划资助项目(批准号:06MA117)
关键词 前列腺癌 EphA1 甲基化 Prostate cancer EphA1 Methylation
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