Biological Effects of High Level c-myc Expression in FR3T3 Fibroblasts

Abstract

The contribution(s) made by the c-myc proto-oncogene to cellular transforation remains obscure and controversial. Introduction of a c-myc gene into primary fibroblast cells facilitates continuous growth in vitro yet these cells retain a normal morphology, are unable to grow in soft agar and, are not tumorigenic in syngeneic hosts or athymic mice (Land et al. 1983; Mougneau et al. 1984; Connan et al. 1985). C-myc activity has also been associated with the competency of cells to enter and progress through the cell cycle (Thompson et al. 1985; Kaczmarek et al. 1985). This picture of c-myc gene function loses its apparent simplicity within the context of cell lines that have been established spontaneously in culture. An activated c-myc gene within certain immortalized cell lines such as Rat2 (Topp 1981) or NIH3T3 (Jainchill et al. 1969) for example, promotes growth in low serum and in soft agar at low efficiency and, converts cells to a tumorigenic phenotype (Keath et al. 1984; Kelekar and Cole 1986). By these latter criteria c-myc could be considered a transforming gene.