Requirement for ras proto-oncogene function during serum-stimulated growth of NIH 3T3 cells (original) (raw)

Nature volume 313, pages 241–243 (1985)Cite this article

Abstract

Human tumours often contain DNA sequences not found in normal tissues which are able to transform cultured NIH 3T3 cells. In some tumours the gene responsible for this transformation belongs to the cellular ras gene family1,2. A specific type of mutation is responsible for converting the cellular proto-oncogene into a ras oncogene capable of inducing transformation3–5. In a study of the function of a cellular ras gene, its protein product (produced in a bacterial cell) was microinjected into NIH 3T3 cells; the recipient cells became morphologically transformed and were induced to initiate DNA synthesis in the absence of added serum6, but only when cellular ras protein was injected at much higher concentrations than required with protein of the transforming ras gene6,7. To further analyse the function of the cellular ras gene, we have now injected monoclonal antibodies against ras proteins into NIH 3T3 cells. We report here that NIH 3T3 cells induced to divide by adding serum to the culture medium are unable to enter the S phase of the cell cycle after microinjection of anti-ras antibody, showing that the protein product of the ras proto-oncogene is required for initiation of the S-phase in NIH 3T3 cells.

This is a preview of subscription content, access via your institution

Access options

Subscribe to this journal

Receive 51 print issues and online access

$199.00 per year

only $3.90 per issue

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Additional access options:

Similar content being viewed by others

References

  1. Parada, L. F., Tabin, C. J., Shih, C. & Weinberg, R. A. Nature 297, 474–478 (1982).
    Article ADS CAS Google Scholar
  2. Santos, E., Tronick, S. R., Aaronson, S. A., Pulciani, S. & Barbacid, M. Nature 298, 343–347 (1982).
    Article ADS CAS Google Scholar
  3. Tabin, C. J. et al. Nature 300, 143–149 (1982).
    Article ADS CAS Google Scholar
  4. Reddy, E. P., Reynolds, R. K., Santos, E. & Barbacid, M. Nature 300, 149–152 (1982).
    Article ADS CAS Google Scholar
  5. Taparowsky, E. et al. Nature 300, 762–765 (1982).
    Article ADS CAS Google Scholar
  6. Stacey, D. W. & Kung, H.-F. Nature 310, 508–511 (1984).
    Article ADS CAS Google Scholar
  7. Feramisco, J. R., Gross, M., Kamata, T., Rosenberg, M. & Sweet, R. W. Cell 38, 109–117 (1984).
    Article CAS Google Scholar
  8. Furth, M. E., Davis, L. J., Fleurdelys, B. & Scolnick, E. M. J. Virol. 43, 294–304 (1982).
    CAS PubMed PubMed Central Google Scholar
  9. Stacey, D. W. & Allfrey, V. G. J. Cell Biol. 75, 807–817 (1977).
    Article CAS Google Scholar
  10. Pledger, W. J., Stiles, C. D., Antoniades, H. W. & Scher, C. D. Proc. natn. Acad. Sci. U.S.A. 74, 4481–4485 (1977).
    Article ADS CAS Google Scholar
  11. Loef, E. B., Wharton, W., Van Wyk, J. J. & Pledger, W. J. Expl Cell Res. 141, 107–115 (1982).
    Article Google Scholar
  12. Land, H., Parada, L. F. & Weinberg, R. A. Nature 304, 596–602 (1983).
    Article ADS CAS Google Scholar
  13. Ruley, H. E. Nature 304, 602–606 (1983).
    Article ADS CAS Google Scholar
  14. Newbold, R. F. & Overell, R. W. Nature 304, 648–651 (1983).
    Article ADS CAS Google Scholar
  15. Waterfield, M. D. et al. Nature 304, 35–39 (1983).
    Article ADS CAS Google Scholar
  16. Doolittle, R. F. et al. Science 221, 275–277 (1983).
    Article ADS CAS Google Scholar
  17. Downward, J. et al. Nature 307, 521–527 (1984).
    Article ADS CAS Google Scholar
  18. Kelly, K., Cochran, B. H., Stiles, C. D. & Leder, P. Cell 35, 603–610 (1983).
    Article CAS Google Scholar
  19. Campisi, J., Gray, H. E., Pardee, A. B., Dean, M. & Sonenshein, G. E. Cell 36, 241–247 (1984).
    Article CAS Google Scholar
  20. Greenberg, M. E. & Ziff, E. B. Nature 311, 433–438 (1984).
    Article ADS CAS Google Scholar
  21. Kruijer, W., Cooper, J. A., Hunter, T. & Verma, I. M. Nature 312, 711–716 (1984).
    Article ADS CAS Google Scholar
  22. Müller, R., Bravo, R., Burkhardt, J. & Curran, T. Nature 312, 716–720 (1984).
    Article ADS Google Scholar
  23. Mercer, W. E., Avignolo, C. & Baserga, R. Molec. cell. Biol. 4, 276–281 (1984).
    Article CAS Google Scholar
  24. Ellis, R. W. et al. Nature 292, 506–511 (1981).
    Article ADS CAS Google Scholar
  25. Shimizu, K. et al. Proc. natn. Acad. Sci. U.S.A. 80, 2112–2116 (1983).
    Article ADS CAS Google Scholar

Download references

Author information

Authors and Affiliations

  1. Department of Cell Biology, Roche Institute of Molecular Biology, Roche Research Center, Nutley, New Jersey, 07110, USA
    Linda S. Mulcahy, Mark R. Smith & Dennis W. Stacey

Authors

  1. Linda S. Mulcahy
    You can also search for this author inPubMed Google Scholar
  2. Mark R. Smith
    You can also search for this author inPubMed Google Scholar
  3. Dennis W. Stacey
    You can also search for this author inPubMed Google Scholar

Rights and permissions

About this article

Cite this article

Mulcahy, L., Smith, M. & Stacey, D. Requirement for ras proto-oncogene function during serum-stimulated growth of NIH 3T3 cells.Nature 313, 241–243 (1985). https://doi.org/10.1038/313241a0

Download citation

This article is cited by