Enhanced cellular radiation sensitivity of androgen-independent human prostate tumor cells by onconase

I Lee1, Y H Lee, S M Mikulski

  • 1Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA. ilee2@mail.med.upenn.edu

Anticancer Research
|May 16, 2000
PubMed

Insights

Onconase, derived from amphibian oocytes, reduces cellular oxygen consumption (QO2) in cancer cells. This finding suggests onconase may enhance radiation therapy effectiveness, particularly for prostate cancer.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Amphibian-derived onconase is known to increase tumor oxygen levels.
  • The mechanism by which onconase affects cellular oxygen consumption (QO2) is not fully understood.

Purpose of the Study:

  • To investigate the effect of onconase on cellular oxygen consumption (QO2) in 9L rat glioma and DU145 human prostate adenocarcinoma cells.
  • To determine if onconase enhances radiation sensitivity in androgen-insensitive prostate cancer cells.

Main Methods:

  • Cellular oxygen consumption (QO2) was measured using a Clark-type electrode chamber.
  • Radiation sensitivity assays were performed on DU145 cells treated with varying concentrations of onconase.

Main Results:

  • Onconase significantly inhibited QO2 in both 9L rat glioma and DU145 human prostate adenocarcinoma cells.
  • Radiation sensitization was observed in DU145 cells at onconase concentrations greater than 5 micrograms/ml, irrespective of p53 status.

Conclusions:

  • Onconase reduces cellular oxygen consumption, potentially increasing oxygen availability to hypoxic tumor cells.
  • Onconase demonstrates potential as a radiosensitizer for androgen-insensitive prostate cancer, warranting further in vivo investigation.

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