The EBV early gene product EB2 transforms rodent cells through a signalling pathway involving c-Myc

Abstract

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with several neoplasia. We present evidence here that the protein EB2, an EBV posttranscriptional activator, has transforming properties not only when expressed in established cell lines such as Rat1 or NIH3T3 but also in primary rat fibroblasts (REF). EB2 transformation in Rat1 cells correlates with an increase in the steady-state level of the cellular oncogenic protein c-Myc, and cotransfection of a plasmid expressing Max suppresses the transformation. These results implicate c-Myc in EB2-mediated cell transformation and help define the pathway by which this EBV early protein causes transformation.