Related Experiment Videos

C127 cells resistant to transformation by tyrosine protein kinase oncogenes

A Cuadrado1, N Talbot, M Barbacid

  • 1Developmental Oncology Section, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701.

Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|January 1, 1990
PubMed

Insights

C127 mouse cells resist transformation by certain oncogenes but can be transformed by others. This resistance is linked to insufficient substrates for tyrosine protein kinase oncogenes.

Area of Science:

  • Cell biology
  • Molecular oncology
  • Cancer research

Background:

  • C127 cells are a standard nontumorigenic mouse cell line for in vitro transformation assays.
  • They exhibit normal morphology and low spontaneous transformation rates, making them suitable for studying oncogene-induced transformation.

Purpose of the Study:

  • To investigate the susceptibility of C127 cells to transformation by different classes of oncogenes.
  • To elucidate the molecular mechanisms underlying C127 cell resistance or sensitivity to specific oncogenes.

Main Methods:

  • Transformation assays using various oncogenes, including tyrosine protein kinase (v-fms, trk, v-src) and serine/threonine kinase (v-mos, v-raf) oncogenes.
  • Generation and analysis of somatic cell hybrids between C127 and NIH3T3 cells.
  • Assessment of transformed phenotypes, including growth in semisolid agar.

Main Results:

  • C127 cells demonstrated resistance to transformation by tyrosine protein kinase oncogenes (v-fms, trk, v-src).
  • Efficient transformation occurred with ras oncogenes and serine/threonine kinase oncogenes (v-mos, v-raf).
  • C127 cells expressing pp60v-src acquired a transformed phenotype after prolonged in vitro passage.
  • Somatic cell hybrids of C127 and NIH3T3 cells expressing p70trk showed transformed properties, unlike hybrids with control C127 cells.

Conclusions:

  • C127 cells possess intrinsic resistance to transformation mediated by specific tyrosine protein kinase oncogenes.
  • This resistance is likely due to a deficiency or low expression of essential substrate(s) for these oncogenes.
  • The findings highlight the importance of specific cellular substrates in oncogenic transformation pathways.

Related Concept Videos