| Ovarian cancer is the fifth most commonly occurring malignancy in North American women, with an overall mortality rate as high as 65% patients. No single causative factor has yet been attributed to ovarian cancer, which has had detrimental implications on our understanding and handling of the disease. EEF1A2, the gene encoding eukaryotic elongation factor 1A2, is amplified in ∼25% of primary ovarian tumours. Furthermore, high expression of EEF1A2 mRNA is detectable in ∼30% of ovarian primary tumours and established ovarian carcinoma cell lines but not in normal ovarian tissue samples or cell lines. We demonstrate that EEF1A2 is a potent cellular oncogene. Expression of eEF1A2 in rodent fibroblasts was sufficient to stimulate focus formation, anchorage-independent growth, increased in vitro growth rate and in vivo tumourigenesis. Similarly, expression of EEF1A2 in a cell culture model of human ovarian cancer enhances the rate of tumour formation in vivo . EEF1A2 does not mediate cellular transformation by means of apoptotic inhibition nor does EEF1A2 effect chemotherapeutic responsiveness. Finally, we find that the oncogenic capacity of EEF1A2 is independent of its function as a translation elongation factor. Rather, eEF1A2 carboxy terminal residues 321-464 are necessary for its oncogenic properties via some uncharacterized function. The discovery of EEF1A2 is an intriguing development in the study of ovarian cancer with exciting potential as a diagnostic marker and molecular target for ovarian cancer therapy. |
