黄利鸣, 邢学森, 黄益玲. p16基因甲基化与HeLa细胞凋亡相关性的研究[J]. 中国肿瘤临床, 2005, 32(13): 721-724.
引用本文: 黄利鸣, 邢学森, 黄益玲. p16基因甲基化与HeLa细胞凋亡相关性的研究[J]. 中国肿瘤临床, 2005, 32(13): 721-724.
Huang Li-ming, Xing Xue-sen, Huang Yi-ling. The Study on Correlation between Methylation of p16 Gene and Apoptosis of Cervical Carcinoma HeLa Cell Induced by Trichosanthin[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(13): 721-724.
Citation: Huang Li-ming, Xing Xue-sen, Huang Yi-ling. The Study on Correlation between Methylation of p16 Gene and Apoptosis of Cervical Carcinoma HeLa Cell Induced by Trichosanthin[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(13): 721-724.

p16基因甲基化与HeLa细胞凋亡相关性的研究

The Study on Correlation between Methylation of p16 Gene and Apoptosis of Cervical Carcinoma HeLa Cell Induced by Trichosanthin

  • 摘要: 目的: 研究天花粉蛋白诱导HeLa细胞凋亡过程中p16基因甲基化的变化情况,探讨细胞凋亡和抑癌基因甲基化的相关性,寻找新的去甲基化药物。 方法: 应用MTT法检测天花粉蛋白对HeLa细胞增殖抑制的影响,流式细胞仪检测天花粉蛋白对HeLa细胞的诱导凋亡作用,甲基化特异PCR(Methylation-specificPCR,MSP)检测HeLa细胞凋亡过程中p16基因启动子区CpG岛的甲基化状况。 结果: 在HeLa细胞中p16基因启动子区CpG岛异常甲基化,经天花粉蛋白处理后,HeLa细胞生长明显受抑,流式细胞仪直方图出现明显的亚二倍体峰,p16基因启动子区CpG岛无异常甲基化表现。 结论: 天花粉蛋白在诱导HeLa细胞凋亡过程中对p16基因有明显的去甲基化作用,可能是新型的去甲基化药物,抑癌基因甲基化失活与肿瘤细胞凋亡之间可能有某些密切的相关性。

     

    Abstract: Objective : To study methylation status of p16 during apoptosis of cervical carcinoma HeLa cell induced by trichosanthin, explore the correlation between cell apoptosis and methylation status of tumor suppressor gene and search for a novel demethlated druggery. Methods : Apoptosis-inducing effect of trichosanthin on cervical carcinoma was detected by MTT and flow cytometry, methylation status of p16 was detected by Methylation-specific PCR. Results : After treatment with TCS, HeLa cells showed a serial of characteristic change of apoptosis, such as the occurrence of subdiploid peak. The CpG island of pig was obvious demethylated. conclusion : Trichosanthin can make p16 obviously demethylated during induction of HeLa cell apoptosis, which is perhaps a novel demethylated druggery.There is a correlation between cell apoptosis and methylation status of tumor suppressor gene.

     

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