Interferon inhibition of DNA synthesis in Swiss 3T3 cells: dissociation from protein kinase C activation.
We have examined the role of protein kinase C in the anti-proliferative effects of interferon in Swiss 3T3 cells. Treatment of these cells with interferon did not stimulate the phosphorylation of an acidic Mr 80,000 cellular protein which serves as a substrate for protein kinase C. In addition, interferon did not inhibit the binding of 125I-epidermal growth factor to specific receptors or induce the expression of the proto-oncogene, c-fos in Swiss 3T3 cells. Thus, interferon does not activate protein kinase C. Moreover, interferon can still inhibit DNA synthesis in protein kinase C down-regulated 3T3 cells, indicating that the presence of this phosphotransferase is not essential for the anti-proliferative effects of interferon.
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology; D002478:Cells, Cultured; D004261:DNA Replication / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D004815:Epidermal Growth Factor / Q000494:pharmacology; D007370:Interferon Type I / Q000502:physiology*; D007700:Kinetics; D051379:Mice; D015240:Phorbol 12,13-Dibutyrate; D010703:Phorbol Esters / Q000494:pharmacology; D010766:Phosphorylation; D011493:Protein Kinase C / Q000378:metabolism*
D002273:Carcinogens; D007370:Interferon Type I; D010703:Phorbol Esters; D015240:Phorbol 12,13-Dibutyrate; D004815:Epidermal Growth Factor; D011493:Protein Kinase C