v-erbA cooperates with bFGF in neuroretina cell transformation

We have studied the transforming ability of the oncogenes erbA and/or erbB in chicken neuroretina (CNR) cells and the effect of basic fibroblast growth factor (bFGF) on the transformed phenotype. The erbA oncogene alone was only transforming in the presence of bFGF. In contrast, cells expressing erbB as well as erbA + erbB were transformed in a bFGF-independent manner and were unresponsive to the growth factor. We studied whether other oncogenes could also block the cooperation between erbA and bFGF. Cytoplasmic or membrane-bound oncogenes (src, ras, or mill raf) increased the transforming potential of erbA but rendered the cells unresponsive to bFGF. Conversely, the nuclear oncogenes tested (fos and myb-ets + myc) also cooperated with erbA in CNR cell transformation but the cells remained responsive to the growth factor. A likely explanation is that CNR cells carrying the cytoplasmic but not the nuclear oncogenes have already activated the bFGF signal transduction pathway.