mPer2在小鼠黑色素瘤细胞B16细胞凋亡中的作用研究

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。

The function of mPer2 on apoptosis of B16 mouse melanoma cell

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: RT-PCR 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 up-regulating the expression of p53 and depressing c-Myc in B16 mouse melanoma cell.