Possible involvement of protein kinase C and calcium ion in growth factor-induced expression of c-myc oncogene in Swiss 3T3 fibroblasts.
Year: 1986
Type: article
Abstract: The addition of platelet-derived growth factor and fibroblast growth factor to quiescent cultures of Swiss 3T3 fibroblasts rapidly induced protein kinase C activation and Ca2+ mobilization and afterwards markedly increased c-myc mRNA levels.1-Oleoyl-2-acetylglycerol, a membrane-permeable synthetic diacylglycerol, and 12-0-tetradecanoylphorbol 13-acetate, a tumor-promoting phorbol ester, stimulated protein kinase C activation without Ca2+ mobilization.Inversely, Ca2+ ionophores, A23187 and ionomycin, elicited Ca2+ mobilization without protein kinase C activation.Both protein kinase C-activating and Ca2+-mobilizing agents were able to increase c-myc mRNA levels in an additive manner.Prolonged treatment of the cells with phorbol 12,13-dibutyrate, another protein kinase Cactivating phorbol ester, led to the down-regulation and complete disappearance of protein kinase C. In these cells, 1-oleoyl-2-acetylglycerol and 12-0-tetradecanoylphorbol 13-acetate did not increase c-myc mRNA levels, but platelet-derived growth factor, fibroblast growth factor, and the Ca2+ ionophores, all of which still induced Ca2+ mobilization, stimulated the increase of c-myc mRNA levels.These results strongly suggest that both protein kinase C and Ca2+ may be involved in platelet-derived growth factoras well as fibroblast growth factor-induced expression of the cmyc oncogene in Swiss 3T3 cells.It has been demonstrated that the c-myc oncogene is rapidly activated after stimulation of mouse lymphocytes by concanavalin A and of BALB/c 3T3 fibroblasts by PDGF,' FGF, and TPA and in regenerating rat liver (1, 2).Moreover, it has been described that expression of the c-myc gene, which is
Source: Journal of Biological Chemistry
Institution: Kobe University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,430
OpenAlex ID: W2098706903