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ELF4/MEF activates MDM2 expression and blocks oncogene-induced p16 activation to promote transformation

Goro Sashida; Yan Liu; Shannon Elf; Yasuhiko Miyata; Kazuma Ohyashiki; Miki Izumi; Silvia Menendez; Stephen D. Nimer (Profiled Author: Yan Liu)

Molecular and Cellular Biology. 2009;29(13):3687-3699.

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 p19^ARF and p16 are increased in Elf4^-/- p53^-/- mef's, and expression of Bmi-1 or knockdown of p16 in this context restores H-Ras^V12-induced transformation. Thus, ELF4/MEF promotes tumorigenesis by inhibiting both the p53 and p16/Rb pathways. Copyright © 2009, American Society for Microbiology. All Rights Reserved.

PMID: 19380490     PMCID: PMC2698769

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