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Updated: Mar 6, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

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p21: A Two-Faced Genome Guardian

Alexandros G Georgakilas1, Olga A Martin2, William M Bonner3

  • 1DNA Damage Laboratory, Physics Department, School of Applied Mathematical and Physical Sciences, National Technical University of Athens (NTUA), Iroon Polytechniou 9, Zografou 15780, Athens, Greece.

Trends in Molecular Medicine
|March 11, 2017
PubMed

Insights

The tumor suppressor p21, typically a guardian of the genome, can also promote cancer in a p53-deficient environment. This dual role has significant implications for cancer therapy and understanding disease progression.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cell Cycle Regulation

Background:

  • The tumor suppressor p53 is activated by DNA damage, inducing p21 expression.
  • p21 (cyclin-dependent kinase inhibitor) typically causes cell cycle arrest, senescence, or apoptosis.
  • p21 presence is often a marker for wildtype p53 activity in clinical settings.

Purpose of the Study:

  • To discuss the dual role of p21 in cancer.
  • To explore the oncogenic functions of p21 in p53-deficient cancers.
  • To consider the implications of p21's multifaceted role in cancer pathogenesis and therapy.

Main Methods:

  • Literature review and discussion of existing evidence.
  • Analysis of the contrasting roles of p21 in different cellular contexts.
  • Speculative analysis based on current research findings.

Main Results:

  • p21 acts as a tumor suppressor in a p53-wildtype context.
  • p21 can function as an oncogene in p53-deficient tumors.
  • p21 may also possess anti-apoptotic functions, complicating its role.

Conclusions:

  • The role of p21 in cancer is context-dependent and paradoxical.
  • Understanding p21's dual function is crucial for developing effective cancer therapies.
  • p21's potential anti-apoptotic activity requires further investigation for therapeutic targeting.
Keywords:
cancererror-prone repairgenomic instabilityp21 overexpressionp53 deficiency

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