Oncogene- transformed NIH 3T3 cells display radiation resistance levels indicative of a signal transduction pathway leading to the radiation-resistant phenotype

Radiat Res. 1993 Aug;135(2):234-43.


Oncogenes and their normal counterparts, proto-oncogenes, are functionally important cellular genes which interact with one another as components of signal transduction pathways leading to cell growth and differentiation. Numerous reports in the literature have also begun to link these genes to the phenomenon of cellular radiation resistance. In this report we examine the radiation resistance level of NIH 3T3 cells transformed by various oncogenes in an attempt to define the intracellular pathway to the radiation-resistant phenotype. The results demonstrate that an analogous signaling pathway is apparently involved in acquisition of radiation resistance. Serine/threonine protein kinase oncogenes such as raf, mos, and PKC play a central role in the pathway. Moreover, specific oncogenes upstream (sis, HER-2, met, trk, and ras) and downstream (ets and myc) of these important signaling mediators can also influence the radiation resistance level of the cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Line, Transformed
  • Cell Survival / radiation effects
  • Mice
  • Nuclear Proteins / metabolism
  • Oncogenes*
  • Phenotype
  • Platelet-Derived Growth Factor / genetics
  • Protein Serine-Threonine Kinases / genetics
  • Protein-Tyrosine Kinases / genetics
  • Radiation Tolerance / genetics*
  • Receptors, Platelet-Derived Growth Factor / metabolism
  • Signal Transduction*


  • Nuclear Proteins
  • Platelet-Derived Growth Factor
  • Protein-Tyrosine Kinases
  • Receptors, Platelet-Derived Growth Factor
  • Protein Serine-Threonine Kinases