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p53-dependent apoptosis modulates the cytotoxicity of anticancer agents

S W Lowe1, H E Ruley, T Jacks

  • 1Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.

Cell
|September 24, 1993
PubMed

Insights

The adenovirus E1A oncogene sensitizes cells to anticancer drugs. The p53 tumor suppressor is essential for cancer cell death, influencing sensitivity and resistance to chemotherapy.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cellular apoptosis

Background:

  • Anticancer drug targets are known, but mechanisms of selective cancer cell death and drug resistance are less understood.
  • The role of p53 in cellular response to anticancer agents requires further systematic investigation.

Purpose of the Study:

  • To investigate the requirement of p53 in cellular sensitivity and resistance to various anticancer agents.
  • To determine if oncogenes can influence cellular responses to chemotherapy.

Main Methods:

  • Utilized p53-deficient mouse embryonic fibroblasts.
  • Examined cellular sensitivity and resistance to ionizing radiation, 5-fluorouracil, etoposide, and adriamycin.

Main Results:

  • The adenovirus E1A oncogene sensitized fibroblasts to apoptosis induced by multiple anticancer agents.
  • The p53 tumor suppressor protein was found to be essential for the efficient execution of the cell death program.
  • Divergent stimuli can activate a common cell death pathway.

Conclusions:

  • The cytotoxic effects of many anticancer agents involve processes beyond initial drug-target interaction.
  • p53's role in apoptosis suggests a mechanism for tumor cells to develop cross-resistance to anticancer drugs.

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