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ELF4/MEF Activates MDM2 Expression and Blocks Oncogene-Induced p16 Activation To Promote Transformation

by Goro Sashida, Yan Liu, Shannon Elf, Yasuhiko Miyata, Kazuma Ohyashiki, Miki Izumi, Silvia Menendez, Stephen D Nimer
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Molecular and Cellular Biology (2009)
Volume: 29, Issue: 13, Publisher: American Society for Microbiology (ASM), Pages: 3687-3699

Abstract

Several ETS transcription factors, including ELF4/MEF, can function as oncogenes in murine cancer models and are overexpressed in human cancer. We found that Elf4/Mef activates Mdm2 expression; thus, lack of or knockdown of Elf4/Mef reduces Mdm2 levels in mouse embryonic fibroblasts (mef's), leading to enhanced p53 protein accumulation and p53-dependent senescence. Even though p53 is absent in Elf4/ p53/ mef's, neither oncogenic H-RasV12 nor c-myc can induce transformation of these cells. This appears to relate to the INK4a/ARF locus; both p19ARF and p16 are increased in Elf4/ p53/ mef's, and expression of Bmi-1 or knockdown of p16 in this context restores H-RasV12-induced transformation. Thus, ELF4/MEF promotes tumorigenesis by inhibiting both the p53 and p16/Rb pathways.

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