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肿瘤细胞中的c-mycp16启动子重新甲基化[J]. 肿瘤防治研究, 2009, 36(09): 730-733. DOI: 10.3971/j.issn.1000-8578.2009.09.003
引用本文: 肿瘤细胞中的c-mycp16启动子重新甲基化[J]. 肿瘤防治研究, 2009, 36(09): 730-733. DOI: 10.3971/j.issn.1000-8578.2009.09.003
De Novo Methylation on c-myc and p16 Promoters in Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2009, 36(09): 730-733. DOI: 10.3971/j.issn.1000-8578.2009.09.003
Citation: De Novo Methylation on c-myc and p16 Promoters in Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2009, 36(09): 730-733. DOI: 10.3971/j.issn.1000-8578.2009.09.003

肿瘤细胞中的c-mycp16启动子重新甲基化

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

  • 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。

     

    Abstract: Objective To explore the effect of de novo methylation of c-myc, p16 promoter regions on the growth of cancer cell line MGC803, and to search a new target for diagnosis and treatment of cancers. Methods MGC803 was exposed to the methyl donor SAM to methylate the promoter regions of c-myc and p16. Growth speed of the cells was evaluated by MTT assay, and the expression of c-myc 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 cells by inhibiting the transcription activity and expression of c-myc without altering the tumor suppressor gene p16, which indicated its function in the treatment of cancer.

     

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