Suppression of E1A-mediated transformation by the p50E4F transcription factor

Elma R. Fernandes, Robert Rooney

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The adenovirus E1A gene can act as an oncogene or a tumor suppressor, with the latter effect generally arising from the induction of apoptosis or the repression of genes that provide oncogenic growth stimuli (e.g., HER- 2/c-erbB2/neu) or increased metastatic invasiveness (e.g., metalloproteases). In this study, coexpression of E1A and p50E4F, a cellular transcription factor whose DNA binding activity is stimulated by E1A, suppressed colony formation by NIH 3T3 cells and transformation of primary rat embryo fibroblasts but had no observed effect in the absence of E1A. Domains in p50E4F required for stimulation of the adenovirus E4 promoter were required for the suppressive effect, indicating a transcriptional mechanism. In serum- containing media, retroviral expression of p50E4F in E1A13S/ras-transformed NIH 3T3 fibroblasts had little effect on subconfluent cultures but accelerated a decline in viability after the cultures reached confluence. Cell death occurred by both apoptosis and necrosis, with the predominance of each process determined by culture conditions. In serum-free media, p50E4F accelerated E1A-induced apoptosis. The results suggest that p50E4F sensitizes cells to signals or conditions that cause cell death.

Original languageEnglish (US)
Pages (from-to)4739-4749
Number of pages11
JournalMolecular and cellular biology
Volume19
Issue number7
DOIs
StatePublished - Jan 1 1999

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Apoptosis
Adenoviridae
Cell Death
Fibroblasts
NIH 3T3 Cells
Serum-Free Culture Media
Metalloproteases
Oncogenes
Genes
Cause of Death
Transcription Factors
Necrosis
Embryonic Structures
DNA
Growth
Serum
rat p50E4F protein
Neoplasms

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

Suppression of E1A-mediated transformation by the p50E4F transcription factor. / Fernandes, Elma R.; Rooney, Robert.

In: Molecular and cellular biology, Vol. 19, No. 7, 01.01.1999, p. 4739-4749.

Research output: Contribution to journalArticle

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