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Cell target genes of Epstein–Barr virus transcription factor EBNA-2: induction of the p55 regulatory subunit of PI3-kinase and its role in survival of EREB2.5 cells

Lindsay C. Spender^1,2,

¹ Department of Virology, Imperial College Faculty of Medicine, Norfolk Place, London W2 1PG, UK
² Ludwig Institute for Cancer Research, University of Tokyo, Tokyo 113-8655, Japan
³ Department of Physiological Chemistry and Metabolism, University of Tokyo, Tokyo 113-8655, Japan
⁴ Institute of Pharmacology, Medical School Hannover, Carl Neuberg Strasse 1, D-30625 Hannover, Germany
⁵ Department of Biochemistry and Molecular Biology, University College London, UK

Correspondence
Paul J. Farrell
p.farrell{at}imperial.ac.uk

Microarray analysis covering most of the annotated RNAs in the human genome identified a panel of genes induced by the Epstein–Barr virus (EBV) EBNA-2 transcription factor in the EREB2.5 human B-lymphoblastoid cell line without the need for any intermediate protein synthesis. Previous data indicating that PIK3R1 RNA (the regulatory subunit of PI3-kinase) was induced were confirmed, but it is now shown that it is the p55 regulatory subunit that is induced. Several EBV-immortalized lymphoblastoid cell lines were shown to express p55. Expression of PI3-kinase p85 regulatory and p110 catalytic subunits was not regulated by EBNA-2. Proliferation of EREB2.5 lymphoblastoid cells was inhibited by RNAi knock-down of p55 protein expression, loss of p55 being accompanied by an increase in apoptosis. p55 is thus a functional target of EBNA2 in EREB2.5 cells and the specific regulation of p55 by EBV will provide an opportunity to investigate the physiological function of p55 in this human cell line.

Present address: Growth Factor Signalling Laboratory, The Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.

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