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Targeting p73 in cancer

Anna-Maria Maas1, Anne Catherine Bretz, Elisabeth Mack

  • 1Molecular Oncology, Department of Hematology, Oncology and Immunology, Institute of Molecular Biology and Tumor Research, Philipps-University Marburg, Marburg, Germany.

Cancer Letters
|September 10, 2011
PubMed

Insights

The tumor suppressor TAp73, crucial for chemotherapy response, is inhibited in cancer cells through reversible mechanisms. Reactivating TAp73 offers a potential therapeutic strategy for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • p73 is a tumor suppressor belonging to the p53 family.
  • Transactivating isoforms of p73 (TAp73) exhibit p53-like anti-proliferative and pro-apoptotic functions essential for chemotherapy.
  • Unlike p53, the TP73 gene is rarely mutated in human cancers, suggesting alternative inactivation mechanisms.

Purpose of the Study:

  • To review how tumor cells inactivate TAp73.
  • To discuss therapeutic strategies for reactivating TAp73 in cancer.

Main Methods:

  • Literature review of TAp73 function and regulation in cancer.
  • Analysis of mechanisms inhibiting TAp73 tumor suppressor activity.
  • Exploration of therapeutic interventions targeting TAp73.

Main Results:

  • TAp73's tumor suppressor activity is inhibited by mechanisms such as epigenetic silencing and complex formation with inhibitory proteins.
  • These inhibitory mechanisms are potentially reversible.
  • TP73 gene mutations are rare in human cancers.

Conclusions:

  • TAp73 plays a vital role as a tumor suppressor, impacting chemotherapy efficacy.
  • Reversible mechanisms inhibit TAp73, presenting opportunities for therapeutic reactivation.
  • Targeting p73 reactivation is a promising strategy for cancer therapy.

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