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作 者:周晓清[1] 马建军[1] 徐晓楠[1] 李磊[1] 甄恩明[1]
机构地区:[1]济宁市第一人民医院口腔颌面外科,272111
出 处:《实用口腔医学杂志》2016年第1期85-88,共4页Journal of Practical Stomatology
基 金:济宁市科技发展计划项目(编号:2014jnwk03)
摘 要:目的:探讨甲基化转移酶抑制剂5-氮杂-2'-脱氧胞苷(5-aza-2'deoxycytidine,5-aza-d C)对腺样囊性癌细胞中RECK基因表达及肿瘤侵袭力的影响。方法:采用甲基化特异性PCR、实时定量PCR、Western印记检测腺样囊性癌细胞中RECK基因的甲基化状态及RECK基因mRNA和蛋白的表达,transwell体外侵袭实验检测细胞侵袭能力。结果:RECK基因甲基化条带仅在ACC-M细胞中发现,经5-aza-d C处理后ACC-M细胞中RECK基因甲基化得到逆转,RECK基因mRNA及蛋白的表达显著提升。ACC-M细胞的侵袭力明显降低。结论:5-aza-d C可逆转腺样囊性癌ACC-M细胞中RECK基因的高甲基化状态并恢复RECK基因mRNA及蛋白的表达,抑制ACC-M细胞侵袭力。Objective: To investigate the effects of 5-aza-2'deoxycytidine(5-aza-dC), a DNA methyhransferase (DNMT) inhibitor, on the methylation status of the RECK gene and the invasion of salivary adenoid cystic carcinoma cell lines. Methods : Methylation- specific PCR, Western blot analysis and quantitative real-time PCR were used to investigate the methy!ation status of RECK gene and the expression of RECK mRNA and protein in SACC cell lines. The invasive ability of SACC Cells was examined by transwell assay. Results: Promoter methylation was only found in ACC-M cell line and not in ACC-2 cell line. Treatment of ACC-M cells with 5-aza- dC partially reversed the hypermethylation status of the RECK gene and significantly enhanced the expression level of mRNA and pro- tein of RECK, suppressed ACC- M cell invasive ability. Condusion: 5- aza- dC can inhibit ACC- M cell invasion by reversal of hyperm- ethylation status of RECK gene.
关 键 词:RECK 腺样囊性癌 5-氮杂-2’-脱氧胞苷(5-aza-dC) 甲基化
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