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P21 and p27: roles in carcinogenesis and drug resistance

Abde M Abukhdeir1, Ben Ho Park

  • 1The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Breast Cancer Research Program, Baltimore, MD, USA.

Expert Reviews in Molecular Medicine
|July 2, 2008
PubMed

Insights

This review examines cyclin-dependent kinase inhibitors p21 and p27, crucial for cell cycle regulation. Their loss is linked to cancer and drug resistance, though they can paradoxically promote tumors.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Human cancers result from dysregulated cell growth and death, governed by cell cycle proteins.
  • Cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors are key regulators of the cell cycle.
  • Loss of G1-checkpoint CDK inhibitors p21 (CDKN1A) and p27 (CDKN1B) is implicated in human malignancies.

Purpose of the Study:

  • To review the identification and function of p21 and p27.
  • To explore the roles of p21 and p27 in carcinogenesis.
  • To analyze the involvement of p21 and p27 in drug resistance.

Main Methods:

  • Literature review of historic and recent studies.
  • Analysis of protein identification and function.
  • Examination of roles in cancer development and drug resistance.

Main Results:

  • Loss of p21 and p27 function is linked to cancer development and progression.
  • Functional loss of p21 and p27 may confer a drug-resistance phenotype.
  • Paradoxical evidence suggests p21 and p27 can also promote tumor growth.

Conclusions:

  • p21 and p27 are critical regulators with complex roles in cell cycle control.
  • Their dysregulation contributes to human carcinogenesis and impacts therapeutic outcomes.
  • Understanding these dual roles is vital for cancer treatment strategies.

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