FOS EXPRESSION INDUCES GROWTH ARREST IN TUMORIGENIC NEURORETINA CELLS

E26-infected chicken neuroretina (CNR) cells expressing P135gag-myb-et s are non-transformed and growth can be stimulated by basic fibroblast growth factor (bFGF). In contrast, MHE226-infected CNR cells, which e xpress p61/63myc in addition to the P135gag-myb-ets of E26, are transf ormed, tumorigenic cells and are growth inhibited by bFGF. We looked f or differences in both cells types which could help to understand the molecular basis of the bFGF response. We found marked differences in c -fos expression. In MHE226-CNR cells c-fos mRNA was induced by 12-0-te tradecanoyl phorbol 13-acetate (TPA) and bFGF, both inhibitors of MHE2 26-infected cell growth. In contrast, serum, a strong growth inducer, did not stimulate c-fos expression. In E26-infected cells all of these factors induced cell growth and c-fos expression. MHE226-CNR cells su perinfected with v-fos(FBJ)-expressing retrovirus were inhibited in th eir growth and unresponsive to bFGF. Introduction of V-fos(FBJ) in E26 CNR cells transformed them but they remained sensitive to bFGF. These results suggest that fos is involved in the induced growth arrest of MHE226-CNR cells.