Malignant transformation of murine fibroblasts by a human c-Ha-ras-1 oncogene does not require a functional epidermal growth factor receptor.
Although mutations in ras genes are thought to be important for the development of about 20% of human tumors, almost nothing is known about the way in which these mutations lead to cellular transformation. The known biochemical properties of the 21-kilodalton ras proteins suggest that they may behave as G proteins, regulating the proliferation of cells in response to growth factor stimulation of a receptor. Although the putative receptor(s) has not been identified, several lines of evidence, in particular the fact that rodent cell lines containing ras oncogenes produce transforming growth factor alpha, have suggested that the epidermal growth factor (EGF) receptor is involved in ras transformation. Here we show that murine fibroblasts with no EGF receptors can be transformed to a completely malignant phenotype with a mutated ras gene. It appears, therefore, that the EGF receptor is not required for ras-mediated transformation of these cells.
D000818:Animals; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D004261:DNA Replication; D066246:ErbB Receptors / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D051379:Mice; D009693:Nucleic Acid Hybridization; D010957:Plasmids; D011519:Proto-Oncogenes; D051381:Rats
D006133:Growth Substances; D066246:ErbB Receptors