| Summary: | 碩士 === 國防醫學院 === 生物化學研究所 === 91 === ABSTRACT
The proto-oncogene c-myc plays a crucial role in the proliferation, apoptosis, and regulation of the cell cycle. Aberrant expression of c-Myc could cause apoptosis, but the detail mechanism of c-Myc-induced apoptosis is still not clear. Myc83 cell line has been established from mammary gland tumors of c-Myc-transgenic mice. In the absence of EGF signaling, a lot of Myc83 cells （50％） undergo apoptosis；in the presence of EGF signaling, only 1.5％ Myc83 cells undergo apoptosis. Therefore, we utilize Myc83 cells to study the mechanism of c-Myc-induced apoptosis. Since anisomycin, an activator of p38 MAPK （mitogen-activated protein kinase）and JNK（c-Jun N-terminal kinase）, can induce apoptosis in Myc83 cells, we also utilize anisomycin treated Myc83 cells as another control. We conclude that caspase-3 is activated, PARP is cleaved, the phosphorylation of ERK1 and ERK2 is inhibited in c-Myc-induced apoptosis. In addition, p53 tumor suppressor gene can be regulated by MDM2. MDM2 inhibits the inactivated p53 protein by binding to p53. The decrease of p53 protein and the increase of MDM2 protein were observed in c-Myc-induced apoptosis.p53 mRNA and MDM2 mRNA both increased in c-Myc-induced apoptosis. We propose that c-Myc induced apoptosis is p53-independent.
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