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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 relationship between methylation of RIZ1 promoter region and ovarian epithelial carcinogenesis. Methods: The ovarian cancer tissue and ovarian cancer cell lines as the research object. MSP was used to detect the methylation status of RIZ1 gene. RT-PCR and Western blot were used to detect the expression of RIZ1 mRNA and protein. Cell proliferation assay was used to detect the proliferation of ovarian cancer cells treated with 5-aza-2’-deoxycytidine. Results: The methylation rates of ovarian cancer tissue, ovarian cancer cell line, benign ovarian tumor tissue and normal ovarian tissue were 25.8%, 40%, 0% and 0% respectively. 5-Aza-2’-deoxycytidine treatment of RIZ1 gene methylation of ovarian cancer cell lines, RIZ1 gene regained expression; and demethylation, ovarian cancer cell growth were slow. Conclusion: The methylation of the tumor suppressor gene RIZ1 promoter is related to the occurrence of epithelial ovarian cancer. DNA methylation is one of the reasons for its expression defect.