肿瘤细胞中的c-myc与p16启动子重新甲基化  

De Novo Methylation on c-myc and p16 Promoters in Cancer Cells

作　　者：李燕妮[1] 王玉川[2] 张维铭[3] 

机构地区：[1]天津市口腔医院中心实验室,300041 [2]天津市眼科医院天津市眼科研究所 [3]天津医科大学实验中心

出　　处：《肿瘤防治研究》2009年第9期730-733,共4页Cancer Research on Prevention and Treatment

摘　　要：目的探讨基因启动子区重新甲基化对肿瘤细胞生长的影响,寻找肿瘤防治新靶点。方法用S-腺苷甲硫氨酸使c-myc和p16启动子甲基化,MTT法测定肿瘤细胞生长状态;免疫荧光染色检测基因表达的变化。结果药物处理后,c-myc表达显著降低(P<0.05),而p16表达无明显变化(P>0.05);肿瘤细胞的生长受到抑制。结论SAM能够通过下调癌基因的表达来抑制肿瘤细胞的生长,提示其在肿瘤治疗方面的应用前景。Objective To explore the effect of de novo methylation of c-myc, p16 promoter regions on the growth of cancer cell line MGCS03, and to search a new target for diagnosis and treatment of cancers. Methods MCK2803 was exposed to the methyl donor SAM to methylate the promoter regions of c-my and p16. Growth speed of the cells was evaluated by MTT assay, and the expression of cmyc and p16 were determined by immunohistochemistry. Results Treated by SAM, MGC803 grew more slowly; the expression of c-myc was obviously decreased （P〈0. 05）. However there was no significant difference in expression of p16 （P〉0. 05）. Conclusion SAM could effectively decrease the growth of the cancer ceils by inhibiting the transcription activity and expression of c-rnyc without altering the tumor suppressor gene p16, which indicated its function in the treatment of cancer.

关 键 词：胃癌细胞系 癌基因 抑癌基因 重新甲基化 

分 类 号：Q52[生物学—生物化学] R730.231[医药卫生—肿瘤]