摘要
背景与目的:抑癌基因启动子异常甲基化是肿瘤发生的重要机理之一,本研究探讨散发性乳腺癌癌变过程14-3-3σ基因启动子异常甲基化状况及其与转录水平的关系。方法:用甲基化特异PCR方法对散发性乳腺癌患者癌组织及正常组织进行14-3-3σ异常甲基化检测;用SYBR greenⅠ实时定量PCR检测14-3-3σmRNA的转录表达。结果:68例散发性乳腺癌组织中,14-3-3σ基因启动子异常甲基化率为90%(61/68),部分不典型增生病例检出异常甲基化15%(2/13),而正常组织未检出甲基化,只检出未甲基化的14-3-3σ。14-3-3σ基因启动子异常甲基化与散发性乳腺癌组织分型、分级和淋巴结转移相关(P<0.05),而与年龄无相关性(P>0.05)。14-3-3σ甲基化与其转录水平呈负相关性(P<0.05)。结论:14-3-3σ基因启动子异常甲基化的检测在散发性乳腺癌癌变过程的组织分型、分级和淋巴结转移等方面有一定的应用价值。14-3-3σ基因启动子异常甲基化是其转录下调乃至缺失的重要原因。
Background and purpose: Hypermethylated alterations of tumor suppressor genes is one important cause of carcinogenesis. In this study, we investigated the relation of 14-3-3σ gene promoter region hypermethylation and its transcription in sporadic breast carcinogenesis. Methods: Hyperrnethylation of 14-3-3σ gene was detected by sensitive MSP assay in carcinous and normal tissue, and its mRNA is also detected by real time PCR. Results: The hypermethylation frequencies of 14-3-3σ were 90 percent in 68 cases of sporadic breast cancer patients. Hypermethylation were presented in portions (2/18) of hyperplastic samples, and no hypermethylation was presented in normal tissue. The hypermethylation change of 14-3-3σ gene was markedly related with various types, grades and lymph node metastases (P 〈 0.05), and no significant differences in methylation frequencies were seen between promenopause and postmenopausc ( P 〉 0.05). The hypermethylation of 14-3-3σ showed reverse relation with its mRNA transcription (P 〈 0.05). Conclusions: Epigeneties alterations of the 14-3-3σ can contribute to reducing or losing transcription of 14-3-3σ protein, which play an important role in the development of sporadic breast carcinomas and involved in various types, grades and lympth node metastases.
出处
《中国癌症杂志》
CAS
CSCD
2007年第4期311-314,共4页
China Oncology
基金
十堰市太和医院中青年科技创新团队资助项目(No:20067D007)。