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Family friction as ΔNp73 antagonises p73 and p53

Sarah G Bailey1, Mark S Cragg, Paul A Townsend

  • 1Human Genetics Division, University of Southampton, School of Medicine, Tremona Road, Southampton SO16 6YD, UK.

The International Journal of Biochemistry & Cell Biology
|January 11, 2011
PubMed

Insights

The tumor suppressor p53 and its homolog p73 regulate cellular responses to DNA damage. However, the p73 isoform ΔNp73 is upregulated in many cancers and may promote tumor growth and treatment resistance.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The p53 and p73 proteins are crucial for maintaining genomic stability and responding to DNA damage.
  • Multiple p73 isoforms exist, potentially with opposing functions, complicating their roles in cellular processes.

Purpose of the Study:

  • To review the literature on the truncated p73 isoform, ΔNp73.
  • To elucidate the unclear cellular functions of ΔNp73.
  • To highlight the role of ΔNp73 in tumorigenesis and treatment resistance.

Main Methods:

  • Literature review of existing studies on p53, p73, and ΔNp73.
  • Analysis of data linking ΔNp73 upregulation to tumor types and treatment outcomes.

Main Results:

  • ΔNp73 is a truncated isoform of p73 lacking the N-terminal transactivation domain.
  • ΔNp73 is upregulated in various primary tumor types.
  • Upregulation of ΔNp73 is associated with pro-tumorigenic activities.

Conclusions:

  • ΔNp73 plays a potentially significant role in cancer development.
  • Understanding ΔNp73 functions is critical for cancer treatment strategies.
  • Further research is needed to fully characterize ΔNp73's mechanisms in tumorigenesis and resistance.

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