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机构地区:[1]广西医科大学第一附属医院,广西南宁530021 [2]广西医科大学基础医学院
出 处:《山东医药》2008年第18期15-16,共2页Shandong Medical Journal
基 金:广西壮族自治区卫生厅立项课题基金资助项目(Z2007077);广西医科大学博士启动基金资助项目(308029)
摘 要:目的探讨表没食子儿茶素没食子酯酸(EGCG)对人膀胱移行细胞癌T24细胞的生长抑制作用及其p16基因表达的影响。方法T24细胞加EGCG培养后,MTT法检测T24细胞抑制率,流式细胞仪DNA含量分析法检测T24细胞周期,巢式甲基特异性PCR法检测EGCG作用前后T24细胞p16基因甲基化状态,RT-PCR法检测T24细胞p16 mRNA。结果与对照组相比,不同浓度EGCG均能明显抑制T24细胞生长,G0-G1期细胞增加;EGCG作用48 h后T24细胞p16 mRNA表达增强,且甲基化程度减弱。结论EGCG可逆转T24细胞p16基因高甲基化状态,显著上调其p16 mRNA表达,将细胞阻滞于G0-G1期。Objective To investigate the effect of epigaltocatechin gallate(EGCG) on growth inhibition in transitional cell carcinoma of bladder cell line T24 and on p16 gene regulation. Methods The T24 cells were cultured with EGCG. The induced growth inhibition of 3724 cell was assayed by MTT. The T24 cell cycle was an,,lyzed by FCM. The methylation status of the p16 gene in T24 cell line before and after treatment with EGCG was detected by the nested -methylation specific PCR. The p16 mRNA of were determined by RT-PCR. Results In comparison to the control, all the three different concentration of EGCG was able to inhibit the growth of T24 cell and increase the cell number in G0 - G1 phase. The p16 mRNA greatly strengthened after 48 h disposal of EGCG,the methylation level was apparently down-regulated. Conclusions EGCG can activate and up-regulate the expression of p16 mRNA which inhibits the proliferation of T24 cell by inducing the G0 - G1 arrest, through inhibiting the methylation of p16 gene.
关 键 词:表没食子儿茶素没食子酯酸 P16基因 膀胱肿瘤 T24细胞 细胞周期
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