摘要
目的:探讨抑癌基因RIZ1启动子区甲基化与卵巢上皮性癌发生的关系。方法:以卵巢癌组织及卵巢癌细胞系为研究对象。MSP检测RIZ1基因甲基化状况;RT-PCR、蛋白印迹分别检测RIZ1mRNA及蛋白表达;细胞增殖实验检测5-杂氮-2'-脱氧胞苷处理卵巢癌细胞前后细胞的增殖状况。结果:卵巢癌组织、卵巢癌细胞系、良性卵巢肿瘤组织及正常卵巢组织中的甲基化率分别为25.8%、40%、0%和0%。5-杂氮-2'-脱氧胞苷处理RIZ1基因发生甲基化的卵巢癌细胞系后,RIZ1基因重新获得表达;且去甲基化处理后,卵巢癌细胞生长均减慢。结论:抑癌基因RIZ1启动子区甲基化与上皮性卵巢癌的发生有关,DNA甲基化是其表达缺陷的原因之一。
Objective: To investigate the correlation between methylation of RIZ1 gene in promoter region and the genesis of epithelial ovarian cancer. Methods: Genomic DNA was isolated from ovarian cancer tissue specimens and ovarian cancer cell lines. Methylation - specific PCR (MSP) was used to check methylation of RIZ1 promoter region. The RIZ1 mRNA expression was detected by RT - PCR and the RIZ1 proptein was examined by Western blot. The demethylating agent, 5 -aza- 2'- deoxycytidine, was used to treat methylated ovarian cancer cells and then, ovarian cancer cell growth was measured in vitro. Results: Methylation indices for ovarian cancer, ovarian cancer cell lines, benign ovarian tumor and normal ovarian tissue were 25. 8%, 40%, 0 and 0 respectively. 5 -aza -2'-deoxycytidine reactivated the expression of RIZ1 in methylated cells and decreased the cell growth in vitro. Conclusion: Methylation of RIZ1 gene is a frequent event in ovarian cancer and is an important mechanism for loss of the gene expression. Aberrant methylation of RIZ1 gene may play a role in the pathogenesis of ovarian cancer.
出处
《中国妇幼保健》
CAS
北大核心
2008年第28期4044-4047,共4页
Maternal and Child Health Care of China