| First Author | Sashida G | Year | 2009 |
| Journal | Mol Cell Biol | Volume | 29 |
| Issue | 13 | Pages | 3687-99 |
| PubMed ID | 19380490 | Mgi Jnum | J:149898 |
| Mgi Id | MGI:3849350 | Doi | 10.1128/MCB.01551-08 |
| Citation | Sashida G, et al. (2009) ELF4/MEF activates MDM2 expression and blocks oncogene-induced p16 activation to promote transformation. Mol Cell Biol 29(13):3687-99 |
| abstractText | 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-Ras(V12) 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. |
