Unravelling mechanisms of p53-mediated tumour suppression

Kathryn T Bieging1, Stephano Spano Mello1, Laura D Attardi2

  • 1Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.

Nature Reviews. Cancer
|April 18, 2014
PubMed

Insights

The tumor suppressor p53 protein controls cell cycle arrest, senescence, and apoptosis. Emerging research reveals p53 also impacts metabolism, metastasis, and the tumor microenvironment, expanding its role in cancer suppression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The p53 protein is a critical tumor suppressor involved in cellular responses to stress.
  • Canonical functions include cell cycle arrest, senescence, and apoptosis, all linked to tumor suppression.

Purpose of the Study:

  • To discuss the established roles of p53 in tumor suppression.
  • To explore emerging functions of p53 beyond its classical stress responses.

Main Methods:

  • Literature review and synthesis of recent findings.
  • Analysis of p53's involvement in diverse cellular processes.

Main Results:

  • Classical p53 functions are well-documented tumor suppressors.
  • Emerging roles in metabolism, stem cell maintenance, invasion, metastasis, and tumor microenvironment modulation are increasingly recognized.

Conclusions:

  • p53's tumor suppressive capacity extends beyond traditional cell cycle control.
  • Understanding these novel functions is crucial for developing new cancer therapies.

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