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p73 cooperates with DNA damage agents to induce apoptosis in MCF7 cells in a p53-dependent manner

J Zhu1, S Nozell, J Wang

  • 1Institute of Molecular Medicine and Genetics Medical College of Georgia, Augusta, Georgia, GA 30912, USA.

Oncogene
|August 9, 2001
PubMed

Insights

The p73 protein sensitizes cancer cells to chemotherapy-induced apoptosis, particularly when interacting with p53. This interaction enhances apoptosis induction, offering potential therapeutic strategies for cancer treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Death Mechanisms

Background:

  • The p53 protein is crucial in cancer therapy, as its apoptosis-inducing function can be enhanced by chemotherapeutic agents.
  • The role of p73, a p53 family member, in sensitizing cancer cells to apoptosis, especially in conjunction with DNA-damaging agents, requires further elucidation.

Purpose of the Study:

  • To investigate whether the p73 protein can sensitize cancer cells to apoptosis induced by DNA-damaging chemotherapeutic agents.
  • To explore the cooperative mechanisms between p73, p53, and DNA-damaging agents in inducing cancer cell death.

Main Methods:

  • Generation of MCF7 adenocarcinoma cell lines with inducible expression of p73 or p53 using a tetracycline-regulated promoter.
  • Treatment of cell lines with chemotherapeutic agents and DNA-damaging agents (e.g., camptothecin).
  • Assessment of apoptosis induction, caspase 2 activation, and p53 target gene promoter activity.

Main Results:

  • At physiological levels, p73, but not p53, sensitized MCF7 cells to apoptosis induced by chemotherapeutic agents.
  • p73 cooperated with camptothecin to activate caspase 2 and with DNA-damaging agents or p53 to induce p53 target genes.
  • The ability of p73 to sensitize cells to apoptosis was abrogated in MCF7E6 cells expressing the human papillomavirus E6 oncogene (p53-null).

Conclusions:

  • A functional interaction between p53 and p73 in MCF7 cells enhances apoptosis induction.
  • p73 plays a significant role in sensitizing cancer cells to DNA damage-induced apoptosis, potentially through caspase 2 activation and cooperation with p53.
  • These findings suggest that targeting p73 and its interaction with p53 could be a viable strategy in cancer therapy.

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