Oncogenic Transformation by Jun
Genes coding for transcription factors make unique oncogenes because of their position in cellular signal transduction. The mechanism of Jun-induced oncogenic transformation emerges as a more complex process than was initially expected. The transforming gene in the avian sarcoma virus 17 (ASV 17) genome is the chicken cell-derived insert jun; the jun sequences excised from ASV 17 and inserted into the expression vector RCAS make this vector oncogenic for chicken embryo fibroblasts. RCAS and similar expression vectors have been widely used to probe the oncogenicity of various mutant jun genes. Cofactors that are activated during wounding and wound healing appear to interact with the transgene to cause oncogenic transformation. Oncogenic transformation seems positioned at the end of this hierarchy, dependent on dimerization, DNA binding, and some form of transcriptional control. Deletion of the major transactivation domain of Jun abolishes the transforming and oncogenic potential of the molecule in mammalian and avian cells.