{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sashida G"],"funding":["NIDDK NIH HHS"],"pagination":["3687-99"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2698769"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(13)"],"pubmed_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-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 path"],"journal":["Molecular and cellular biology"],"pubmed_title":["ELF4/MEF activates MDM2 expression and blocks oncogene-induced p16 activation to promote transformation."],"pmcid":["PMC2698769"],"funding_grant_id":["R01 DK052208","R01 DK52208"],"pubmed_authors":["Liu Y","Izumi M","Sashida G","Miyata Y","Elf S","Ohyashiki K","Menendez S","Nimer SD"],"additional_accession":[]},"is_claimable":false,"name":"ELF4/MEF activates MDM2 expression and blocks oncogene-induced p16 activation to promote transformation.","description":"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 path","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Jul","modification":"2025-04-19T10:30:25.627Z","creation":"2019-03-27T00:23:02Z"},"accession":"S-EPMC2698769","cross_references":{"pubmed":["19380490"],"doi":["10.1128/MCB.01551-08","10.1128/mcb.01551-08"]}}