1. ¹Medical Genetics, School of Molecular and Clinical Medicine, University of Edinburgh, Molecular Medicine Centre, Western General Hospital, Edinburgh EH4 2XU, UK
2. ²Cancer Research UK, Edinburgh Oncology Unit, University of Edinburgh Cancer Research Centre, Edinburgh EH4 2XR, UK
3. ³Division of Pathology, University of Edinburgh, Royal Infirmary, Little France, Edinburgh EH4 2XR, UK

Correspondence: Dr CM Abbott, E-mail: C.Abbott@ed.ac.uk

⁴Present address: Department of Cancer Medicine, Imperial College London, Room 1002 Cancer Centre, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK.

Received 1 December 2006; Revised 16 March 2007; Accepted 21 March 2007; Published online 17 April 2007.

Abstract

The tissue-specific translation elongation factor eEF1A2 is a potential oncogene that is overexpressed in human ovarian cancer. eEF1A2 is highly similar (98%) to the near-ubiquitously expressed eEF1A1 (formerly known as EF1-) making analysis with commercial antibodies difficult. We wanted to establish the expression pattern of eEF1A2 in ovarian cancer of defined histological subtypes at both the RNA and protein level, and to establish the mechanism for the overexpression of eEF1A2 in tumours. We show that while overexpression of eEF1A2 is seen at both the RNA and protein level in up to 75% of clear cell carcinomas, it occurs at a lower frequency in other histological subtypes. The copy number at the EEF1A2 locus does not correlate with expression level of the gene, no functional mutations were found, and the gene is unmethylated in both normal and tumour DNA, showing that overexpression is not dependent on genetic or epigenetic modifications at the EEF1A2 locus. We suggest that the cause of overexpression of eEF1A2 may be the inappropriate expression of a trans-acting factor. The oncogenicity of eEF1A2 may be related either to its role in protein synthesis or to potential non-canonical functions.