期刊
ONCOGENE
卷 20, 期 28, 页码 3746-3750出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1204466
关键词
c-Myc; apoptosis; growth factors; Akt
资金
- NCI NIH HHS [CA71874] Funding Source: Medline
A conditionally active chimeric form of the c-Myc protein fused to the ligand-binding domain of the estrogen receptor (MycER) was expressed in PC12 cells, Induction of Myc activity resulted in a threefold increase in apoptosis after 5 days when cells were maintained in 1% serum, The effect of Myc overexpression was dependent on its DNA-binding domain but not on its heterodimeric binding protein Max, which is absent in PC12 cells, Preincubation of the c-Myc overexpressing cells with either NGF or bFGF, but not EGF, prevented the Myc-mediated increase in apoptosis, although the signaling pathways used by NGF and bFGF to block cell death differed, NGF-mediated rescue was mediated by the phosphatidylinositol 3 ' -OH (P13) kinase/Akt pathway white rescue by bFGF was not affected by P13 kinase inhibitors, These results show that Myc can induce apoptosis in PC12 cells in a Max-independent manner and that alternate signaling pathways exist to mediate cell survival.
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