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Related Experiment Videos

Cyclin expression and G2-phase delay after irradiation

E J Bernhard1, W G McKenna, R J Muschel

  • 1Department of Radiation Oncology, University of Pennsylvania, Philadelphia 19104.

Radiation Research
|April 1, 1994
PubMed
Summary
This summary is machine-generated.

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Oncogenes H-ras and v-myc together increase radiation resistance in fibroblasts more than alone. This resistance is linked to a longer G2-phase delay, affecting cell cycle progression and cyclin B expression.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Radiation Biology

Background:

  • Oncogene transfection impacts cellular radiation sensitivity.
  • Primary rat embryo fibroblasts are a model for studying radiation effects.

Purpose of the Study:

  • To investigate the combined effect of H-ras and v-myc oncogenes on radiation resistance.
  • To explore the relationship between G2-phase delay and radiation sensitivity.
  • To examine cyclin B expression during the cell cycle after irradiation.

Main Methods:

  • Oncogene transfection of primary rat embryo fibroblasts.
  • Assessment of radiation sensitivity and G2-phase delay.
  • Analysis of cyclin B mRNA and protein levels post-irradiation.

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Main Results:

  • Combined H-ras plus v-myc transfection conferred greater radiation resistance than single oncogenes.
  • Radioresistant cells exhibited a prolonged G2-phase delay.
  • Irradiation reduced cyclin B mRNA in S phase and cyclin B protein in G2 phase.

Conclusions:

  • Co-expression of H-ras and v-myc oncogenes induces significant radioresistance.
  • G2-phase delay is a key determinant of radiation sensitivity.
  • Regulation of cyclin B expression is involved in radiation-induced G2-phase arrest.