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Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene

B J Ledwith1, S Manam, A R Kraynak

  • 1Merck Sharp & Dohme Research Laboratories, West Point, Pennsylvania 19486.

Molecular and Cellular Biology
|April 1, 1990
PubMed

Insights

Inhibiting c-fos gene expression partially reversed cancer cell transformation caused by the ras oncogene. This suggests c-fos is crucial in ras-regulated growth pathways.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The c-Ha-ras oncogene drives cell proliferation and transformation.
  • c-fos is hypothesized to function downstream of c-Ha-ras in growth signaling.

Purpose of the Study:

  • To investigate the role of c-fos in ras-induced cell transformation.
  • To determine if inhibiting c-fos affects the phenotypes of NIH 3T3 cells expressing the EJ c-Ha-ras oncogene.

Main Methods:

  • Utilized antisense RNA to specifically inhibit c-fos gene expression.
  • Employed immunofluorescent staining to quantify c-fos protein levels.
  • Assessed transformed cell phenotypes, including growth control, morphology, and tumorigenicity.

Main Results:

  • Antisense RNA significantly reduced c-fos protein expression in EJ cells.
  • Inhibition of c-fos partially restored density-dependent growth arrest and serum-induced quiescence.
  • c-fos inhibition led to a flatter cell morphology, reduced anchorage-independent growth, and decreased tumorigenicity in nude mice.

Conclusions:

  • c-fos activity is essential for the full expression of ras-induced oncogenic phenotypes.
  • Inhibiting c-fos can counteract the transforming effects of the ras oncogene, even with continued ras overexpression.
  • These findings support the role of c-fos in ras-mediated signal transduction pathways regulating cell growth and transformation.

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