Insulin/insulin-like growth factor I induce actin transcription in mouse fibroblasts expressing constitutively myc gene

Abstract

Quiescent benzo[α]pyrene-transformed BALB/c 3T3 fibroblasts (line BP-A31), continue to express ‘competence’ genes (such as c- myc) and do not require platelet-derived growth factor (‘competence’ factor) in order to resume the cell division cycle. Insulin-like growth factor I (IGF-I), as well as insulin (at high concentrations, where it interacts with IGF-I-receptors) are potent mitogens in these cells. In contrast with the original non-transformed A31 cell line, we show that insulin/IGF-I (even in the absence of de novo protein synthesis) induce actin transcription in BP-A31 cells. We have verified that ‘CArG’ boxes, major actin promoter elements, can act as insulin-inducible elements in BP-A31 cells. Insulin-induced actin transcription is also observed in quiescent A31 cells stably transfected with a myc expression vector, suggesting a correlation between constitutive myc expression and insulin-induced actin transcription.