The effect of pertussis toxin (PT) on transforming growth factor beta 1 (TGF beta 1)-induced proto-oncogene expression was investigated in AKR-2B fibroblasts. PT substantially abolished c-sis and c-myc mRNA expression following TGF beta 1 stimulation. This inhibitory effect was specific for TGF beta 1-stimulated proto-oncogene expression and associated with the ADP-ribosylation of a 41-kDa substrate. Actinomycin D decay and nuclear run-on experiments demonstrated that the inhibitory effects of PT are a result of decreased transcriptional activation and not to an increased decay of proto-oncogene message. PT did not, however, affect TGF beta 1-stimulated fibronectin and collagen mRNA accumulation nor did it have any inhibitory effect on TGF beta 1-induced morphological transformation. These data indicate that TGF beta 1-stimulated gene expression is coupled to multiple pathways distinguished by their sensitivity to PT.
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Howe et al. (1990) studied this question.