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c-fos and Growth Control

  • R. Müller
  • R. Bravo
Part of the Colloquium der Gesellschaft für Biologische Chemie 10.–12. April 1986 in Mosbach/Baden book series (MOSBACH, volume 37)

Abstract

It is now generally accepted that the normal cellular homologues of retroviral oncogenes, the proto-oncogenes, may have crucial physiological functions in the regulation of cellular proliferation. This hypothesis is strongly supported by the observation that three proto-oncogenes, c-sis, c-erbB and c-fms are part of the cellular growth factor-receptor system (Doolittle et al. 1983, Waterfield et al. 1985, Downward et al. 1984, Sherr et al. 1985). In addition, expression of proto-oncogenes encoding nuclear proteins has been shown to increase rapidly following the stimulation of different cell types using several mitogenic agents: The transient transcriptional activation of the c-fos gene is followed by the accumulation of c-myc RNA (Kelly et al. 1983, Greenberg and Ziff 1984, Cochran et al. 1984, Kruijer et al. 1984, Miiller et al. 1984). This article summarizes the available data suggesting an early role for c-fos in inducing the “competent state” in fibroblasts and thus in the movement of quiescent cells into the cell cycle. In addition, we will discuss the signal transduction pathways that seem to be involved in the induction of c-fos by growth factors.

Keywords

NIH3T3 Cell Quiescent Cell Competent State Progression Factor Phospholipid Degradation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Armelin HA, Armelin MCS, Kelly K, Stewart T, Leder P, Cochran BH, Stiles CD (1984) Functional role for c-myc in mitogenic response to platelet-derived growth factor. Nature (London) 310:655–660CrossRefGoogle Scholar
  2. Berridge MJ, Irvine RF (1984) Inositol triphosphate, a novel second messenger in cellular signal transduction. Nature (London) 312:315–321CrossRefGoogle Scholar
  3. Bravo R, Burckhardt J, Müller R (1985) Persistence of the competent state in mouse fibroblasts is independent of c-fos and c-myc expression. Exp Cell Res 160:540–543PubMedCrossRefGoogle Scholar
  4. Bravo R, Burckhardt J, Müller R (1986) Expression of c-fos in NIH3T3 cells is very low but inducible throughout the cell cycle. EMBO J 5:695–700PubMedGoogle Scholar
  5. Cochran BH, Reffel AC, Stiles CD (1983) Molecular cloning of gene sequences regulated by platelet-derived growth factor. Cell 33:939–947PubMedCrossRefGoogle Scholar
  6. Cochran BH, Zullo J, Verma IM, Stiles CD (1984) Expression of the c-fos oncogene and a newly discovered r-fos is stimulated by platelet-derived growth factor. Science 226:1080–1082PubMedCrossRefGoogle Scholar
  7. Doolittle RF, Hunkapillar MW, Hood LE, Deware SGf Robbins KC, Aaronson SA, Antoniades HN (1983) Simian sarcoma virus onc gene, v-sis, is derived from the gene (or genes) encoding a platelet-derived growth factor. Science 221:275–277PubMedCrossRefGoogle Scholar
  8. Downward J, Yarden Y, Mayes E, Scrace G, Totty N, Stockwell P, Ullrich A, Schlessinger J, Waterfield MD (1984) Close similarity of epidermal growth factor and v-erB oncogene protein sequence. Nature (London) 307:521–527CrossRefGoogle Scholar
  9. Greenberg ME, Ziff EM (1984) Stimulation of 3T3 cells induces transcription of the c-fos proto-oncogenes. Nature (London) 311:433–438CrossRefGoogle Scholar
  10. Kelly K, Cochran BH, Stiles CD, Leder P (1983) Cell-specific regulation of the c-myc gene by lymphocyte mitogens and platelet-derived growth factor. Cell 35:603–610PubMedCrossRefGoogle Scholar
  11. Kruijer W, Cooper JA, Hunter T, Verma IM (1984) Platelet-derived growth factor induces rapid but transient expression of the c-fos gene and protein. Nature (London) 312:711–716CrossRefGoogle Scholar
  12. Lau LF, Nathans D (1985) Identification of a set of genes during the Go/Gl transition of cultured mouse cells. EMBO J 4:3145–3151PubMedGoogle Scholar
  13. Müller R, Bravo R, Burckhardt J, Curran T (1984) Induction of c-fos gene and protein by growth factors precedes activation of c-myc. Nature (London) 312:716–720CrossRefGoogle Scholar
  14. Nishizuka Y (1984) The role of protein kinase C in cell surface signal transduction and tumour promotion. Nature (London) 308:693–698CrossRefGoogle Scholar
  15. Sherr CJ, Rettenmier CW, Sacca R, Roussel MF, Look AT, Stanley ER (1985) The c-fms proto-oncogene product is related to the receptor for the mononuclear phagocyte growth factor, CSF-1. Cell 41:665–676PubMedCrossRefGoogle Scholar
  16. Singh JP, Chaikin MA, Pledger WJ, Scher CD, Stiles CD (1982) Persistence of the mitogenic response to platelet-derived growth factor (competence) does not reflect a long-term interaction between the growth factor and the target cell. J Cell Biol 96:1497–1502CrossRefGoogle Scholar
  17. Stiles CD, Capone GT, Scher CD, Antoniades HN, Van Wyk JJ, Pledger WJ (1979) Dual control of cell growth by somatomedins and platelet-derived growth factor. Proc Natl Acad Sci USA 76:1279–1283PubMedCrossRefGoogle Scholar
  18. Verrier B, Miiller D, Bravo R, Müller R (1986) Wounding a fibroblast monolayer results in the rapid induction of the c-fos proto-oncogene. EMBO J 5:913–917PubMedGoogle Scholar
  19. Waterfield MD, Scrace GT, Whittle N, Stroobant P, Johnsson A, Westeson A, Westermark B, Helding C-H, Huang JS, Deuel TF (1983) Platelet-derived growth factor is structurally related to the putative transforming protein p28sis of simian sarcoma virus. Nature (London) 304:35CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

  • R. Müller
  • R. Bravo
    • 1
  1. 1.European Molecular Biology LaboratoryHeidelbergGermany

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