EBER1 - Oncogenic in Vivo?

Repellin, C. and Wilson, J. B. (2006) EBER1 - Oncogenic in Vivo? 12th International EBV Symposium, Boston, MA, USA, 08-12 Jul 2006.

Abstract

Transfection of the EBERs into Epstein-Barr virus negative Akata cells, which were shown to lose the malignant phenotype and resistance to apoptosis present in EBV positive Akata cells, restored these properties. Thus suggesting an oncogenic role of the EBERs in Burkitt’s lymphoma cells and therefore indicating their possible contribution to the disease process of EBV-associated tumours (Komano et al., 1999). Furthermore, Yajima et al., (2005) have recently reported that the EBERs contribute to the transformation process of EBV in primary B cells. In order to investigate the action of EBER1 as a potential oncogenic RNA, we have generated 13 lines of transgenic mice designed to express EBER1 in lymphoid cells. The transgenes incorporate a novel combination of tissue-specific RNA polymerase II and polymerase III elements and their expression was first confirmed in culture. Mice of 10 of the transgenic lines have been shown to express EBER1 with specificity towards lymphoid tissues. Mice expressing EBER1 are viable. The phenotypic consequences of EBER1 expression in vivo is being examined and lymphoid expansion in mice of several lines has been observed at a young age as well as the development of B-cell lymphoma in one of the lines to date. The role of EBER1 in response to dsRNA stimulation in vivo is under study. Cross-breeding programmes were undertaken which revealed cooperation in B-cell lymphomagenesis between EBER1 and N-myc although this was not evident with the highly tumourigenic c-Myc line. This might suggest that the oncogenic predisposition in the EBER mice is elicited through a cell survival mechanism. The results in this study support the hypothesis that EBER1 has oncogenic properties, the first polymerase III RNA described as such. Thus implicating the RNA in the pathogenesis of EBV associated lymphoma in addition to, or possibly as a consequence of, its role in immune evasion.

• Item Type: Conference or Workshop Item
• Status: Published
• Refereed: No
• Glasgow Author(s) Enlighten ID: Wilson, Professor Joanna
• Authors: Repellin, C., and Wilson, J. B.
• Subjects: Q Science > QR Microbiology > QR355 Virology
• College/School: College of Medical Veterinary and Life Sciences > School of Life Sciences; College of Medical Veterinary and Life Sciences > School of Molecular Biosciences

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