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mPer2在小鼠黑色素瘤细胞B16细胞凋亡中的作用研究

The function of mPer2 on apoptosis of B16 mouse melanoma cell
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摘要 目的:研究mPer2在小鼠黑色素瘤细胞B16细胞凋亡中的作用机制。方法:将构pcDNA3.1-mper2和pcDNA3.1空质粒分别转染入小鼠黑色素瘤细胞B16中。提取两组细胞的总RNA和总蛋白,利用特异引物和抗体,分别检测两组细胞中p53和c-Myc基因在RNA和蛋白水平表达的变化。结果:RT-PCR和蛋白印迹检测均显示与转染pcDNA3.1(+)空质粒相比,转染pcDNA3.1-mPer2入B16细胞后,p53的表达增高,而c-Myc表达降低。结论:mPer2可能通过抑制细胞癌基因c-Myc的表达,促进抑癌基因p53的表达,从而抑制B16细胞生长,诱导细胞凋亡。 Objective. To study the function of mPer2 on apotosis of B16 mouse melanoma cell. Methods: pcDNA 3. 1-mPer2 plasmids and pcDNA 3. 1 plasmids were transfected into mouse melanoma sell B16, Total RNA and protein were extracted from two groups. Special primer of p53 and c-Myc were designed to test the expression of p53 and c-Myc in each group of B16. The special antibody of p53 and c-Myc also were used to check the expression of p53 and c-Myc on protein level in these two groups. Results: RTPCR and western-blot of p53 and c-Myc showed that the p53 gene expression was up-regulation and c-Myc was depressed in pcDNA 3. 1 mPer2 group. Conclusion, The function of mPer2 depressing B16 cell growth and induced it into apotosis maight be through upregulating the expression of p53 and depressing c-Myc in B16 mouse melanoma cell.
出处 《四川生理科学杂志》 2006年第4期161-163,共3页 Sichuan Journal of Physiological Sciences
关键词 mPer2 P53 C-MYC B16细胞 细胞凋亡 mPer2 p53 c-Myc B16 cell liner Apotosis
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