Abstract
A cDNA clone covering part of fhe C-terminal domain of human EF-1δ was isolated from mammary cancer cells by subtractive hybridisation. The higher expression of EF-1δ in the tumours suggested that malignant transformation in vivo requires an increase in translation factor mRNA and protein synthesis for entry into and transition through the cell cycle. To explore the relation between cell division and EF-1δ expression, MCF-7 cells were treated with dexamethasone, an inducer of differentiation. There was no change in the mRNA levels of EF-1δ in the dexamethasone-treated cells. To explore the relation between oncogenes and EF-1δ expression, a variety of oncogenes were introduced into human mammary epithelial cells (MCF-7) and human keratinocytes (HaCaT). Despite high oncogene mRNA expression, there was no significant change in the EF-1δ mRNA level by v-src, c-erbB (EGF Receptor), c-erbB-2, v-myc and v-fos oncogenes. However, overexpression of v-Ha-ras in HaCaT cells resulted in a three to five-fold decrease in the steady-state mRNA level of EF-1δ. Taken together, the data provides further support on the interaction of translation factors and oncogenic transformation.
Original language | English (US) |
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Pages (from-to) | 385-392 |
Number of pages | 8 |
Journal | Anticancer research |
Volume | 18 |
Issue number | 1 A |
State | Published - Jan 1998 |
Keywords
- Elongation factor-1delta (EF-1δ)
- Epithelial cells
- Oncogenes
- Transformation
- Translation
ASJC Scopus subject areas
- Oncology
- Cancer Research