Human E2F5 gene is oncogenic in primary rodent cells and is amplified in human breast tumors.

Détails

ID Serval
serval:BIB_F8B83C013480
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Human E2F5 gene is oncogenic in primary rodent cells and is amplified in human breast tumors.
Périodique
Genes, Chromosomes and Cancer
Auteur(s)
Polanowska J., Le Cam L., Orsetti B., Vallés H., Fabbrizio E., Fajas L., Taviaux S., Theillet C., Sardet C.
ISSN
1045-2257 (Print)
ISSN-L
1045-2257
Statut éditorial
Publié
Date de publication
2000
Volume
28
Numéro
1
Pages
126-130
Langue
anglais
Résumé
E2F transcription factors (E2F1 to 6) are central players in the control of animal cell proliferation as regulators of genes involved in cell cycle progression and in transformation. In this report, we have investigated the potential involvement of the E2F5 gene in tumorigenesis. We show that E2F5 can promote the formation of morphologically transformed foci in primary baby rat kidney cells (BRK) when it is overexpressed in the presence of its heterodimeric partner DP1 and activated RAS. This suggests that E2F5 behaves like a MYC-type cooperating oncogene in functional assays, prompting us to monitor potential amplifications of the E2F5 gene in primary human tumors. We mapped the human E2F5 gene to 8q21.1-21.3 equidistant from the MOS (8q12) and MYC (8q24) oncogenes. Since the long arm of chromosome 8 is frequently the site of increased gene copy number (ICN) in breast cancer, we screened 442 breast tumor DNAs for gains of E2F5, MOS, and MYC genes. The three genes showed ICN, albeit at variable incidence and levels of amplification, with the ICN of E2F5 occurring concomitantly with those of MOS and/or MYC in almost half of the cases. Moreover, a marked increase of the 2. 5-kb E2F5 transcript was also detected in some tumors and tumor cell lines. In conclusion, the evidence that sustained unregulated expression of E2F5 can cooperate with other oncogenes to promote cell transformation in functional assays, together with the detection of chromosomal amplifications and overexpressions of the E2F5 gene in breast tumors, provides the first indications that E2F5 deregulation may have a role in human tumor development.
Mots-clé
Animals, Breast Neoplasms/genetics, E2F5 Transcription Factor, Gene Amplification/genetics, Gene Dosage, Humans, Oncogenes/genetics, Rats, Rats, Sprague-Dawley, Transcription Factors/biosynthesis, Transcription Factors/genetics, Tumor Cells, Cultured
Pubmed
Web of science
Création de la notice
07/03/2013 17:09
Dernière modification de la notice
03/03/2018 22:52
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