Abstract
Lee and his co-workers1, 2 claimed that reovirus selectively killed cells with an activated Ras pathway: activated Ras or an activated element of the Ras pathway inhibited double-stranded RNA-activated protein kinase (PKR) activation, thereby allowing viral protein synthesis. Reovirus remains actively pursued as a potential anticancer agent. We have examined the reovirus-induced cytopathic effect (CPE) in eight human tumor cell lines. Untransformed NIH/3T3 and LLC-MK2 cell lines served as controls. NIH/3T3 is a mouse fibroblast cell line;3 the LLC-MK2 cell line was derived from kidneys of adult Rhesus monkeys.4 Reovirus serotype 3 can infect LLC-MK2, many human tumor cell lines and several untransformed murine cell lines such as L929,5 but not NIH/3T3. We sought to correlate CPE, and intracellular viral RNA measured by polyacrylamide gel electrophoresis, with relative Ras protein levels in the individual cell lines, measured by western blotting. In addition, attempts were made to correlate virus-induced translational control pathways with CPE by immunoblotting for total and phosphorylated double-stranded RNA-activated protein kinase and phosphorylated eukaryotic initiation factor-2α (eIF-2α).6
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