摘要
目的探讨突变型与野生型c-myc基因在非p53依赖性通路中对Bim基因表达调控及细胞凋亡的诱导功能。方法分别用携带突变型与野生型c-myc基因慢病毒载体感染p53缺失型乳癌HCC1937细胞,并得到二者过表达的稳定细胞株,以未感染组及感染不携带c-myc基因的慢病毒细胞做空白对照和感染对照,RT-PCR检测突变型与野生型c-myc及Bim基因mRNA表达,MTT、TUNEL检测突变型与野生型c-myc基因过表达乳癌HCC1937细胞增殖与凋亡情况。结果 RT-PCR结果显示,突变型组与野生型组c-myc基因mRNA过表达,野生型组Bim基因mRNA表达量与突变型组比较,差异有显著性(F=125.191、157.974,P<0.05)。突变型组细胞增殖活性显著高于野生型组(F=769.64,P<0.05)。突变型组与两对照组细胞凋亡率较低,三者相比差异无显著性,野生型组细胞凋亡率显著高于突变型组与两对照组(F=61.57,P<0.05)。结论非p53依赖性通路中,野生型c-myc基因过表达能明显上调Bim基因表达,通过Bim诱导细胞凋亡,而突变后此作用丧失,致瘤性增高。
Objective To investigate the regulation of Bim expression and induction of cell apoptosis of mutant and wildtype c-myc in non-p53-dependent pathway. Methods The mutant and wild type c-myc genes were transfected into HCC1937 by lentivirus, a stable overexpression eel1 line was obtained. Uninfected and cells infected with lentivirus without carrying c-myc gene were served as blank control and infection control Mutant and wild-type c-myc overexpressions and apoptosis in HCC1937 cells were detected by MTT and TUNEL, respectively. Results In mutant group and wild-type group, c-myc mRNA was overex- pressed, the difference of Bim mRNA between mutant and wild-type group was significant （F=125.191,157.974 ; P〈0.05）. The activity of cell multiplication in mutant group was stronger than that in wild-type group （F= 769. 64, P〈0.05）. The apoptosis rates in mutant group and the two control groups were low, with no significant differences among them, and that in wild-type group, the apoptosis was higher than that in mutant group and the other two control groups （F=61.57,P〈0.05）. Conclusion In non-p53-dependent pathway, the overexpression of wild-type c-myc obviously up-regulates and induces cell apoptosis. This action will lose after mutation of c-myc, and it increases oncogenicity.
出处
《齐鲁医学杂志》
2012年第5期395-397,400,共4页
Medical Journal of Qilu
基金
山东省自然科学基金资助项目(Y2007C134)
