P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor.
The viral oncogene v-ras inhibited the platelet-derived growth factor (PDGF)-induced upregulation of c-myc and c-fos proto-oncogene expression in fibroblast monolayers. These v-ras-containing cells proliferated in the absence of c-myc induction and no longer required PDGF to support growth. Fibroblasts expressing v-ras continued to express the same number of functional PDGF receptors on their surface as uninfected cells, yet the usual induction of transcription of the genes c-myc, c-fos, and JE in response to PDGF stimulation did not occur in the presence of newly introduced v-ras or chronic v-ras gene expression, and synthesis of c-myc protein did not occur. This inhibitory effect on growth factor-mediated induction of cellular proto-oncogenes was specific for PDGF in that induction of the c-myc and c-fos genes by certain other factors was not impaired.
Zullo
J N
JN
Division of Pediatric Hematology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115.
Faller
D V
DV
D000818:Animals; D002460:Cell Line; D002478:Cells, Cultured; D005786:Gene Expression Regulation / Q000187:drug effects; D005814:Genes, Viral; D011905:Genes, ras; D007700:Kinetics; D008565:Membrane Proteins / Q000235:genetics*; D051379:Mice; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology*; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000502:physiology; D016283:Proto-Oncogene Proteins p21(ras); D011519:Proto-Oncogenes / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics; D011956:Receptors, Cell Surface / Q000502:physiology; D017479:Receptors, Platelet-Derived Growth Factor; D014158:Transcription, Genetic / Q000187:drug effects
D008565:Membrane Proteins; D010982:Platelet-Derived Growth Factor; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D017479:Receptors, Platelet-Derived Growth Factor; D016283:Proto-Oncogene Proteins p21(ras)