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Related Experiment Videos

Multiple stress signals induce p73beta accumulation.

Kai Wei Lin1, Shin Yuen Nam, Wen Hong Toh

  • 1Laboratory of Molecular Carcinogenesis, National Cancer Centre, 11 Hospital, Drive, Singapore 169610, Singapore.

Neoplasia (New York, N.Y.)
|November 19, 2004
PubMed
Summary
This summary is machine-generated.

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The tumor suppressor p73, unlike p53, is not frequently mutated in cancers. Stress signals like UV irradiation upregulate p73, promoting cancer cell apoptosis and offering a potential therapeutic strategy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Stress Response

Background:

  • p73 is a homologue of the tumor suppressor p53 but is not frequently mutated in human cancers.
  • p73 responds to a limited set of p53-activating signals, but not all genotoxic stresses that induce p53-independent cell death.

Purpose of the Study:

  • To investigate the regulation of p73 by various stress stimuli.
  • To determine the role of p73 in stress-induced apoptosis.
  • To explore therapeutic strategies targeting cancers with unmutated p73.

Main Methods:

  • Utilized a p73-specific antibody to assess p73 protein levels.
  • Examined p73 mRNA and protein stability under various stress conditions (UV irradiation, sorbitol, hydrogen peroxide, nocodazole, taxol).

Related Experiment Videos

  • Assessed apoptosis in cells expressing a dominant-negative p73 inhibitor (p73DD) and p73(-/-) fibroblasts.

    • Main Results:

    • Confirmed c-Abl's requirement for cisplatin-induced p73 upregulation.
    • Demonstrated p73 upregulation by UV irradiation and other stress stimuli.
    • Showed that stress signals regulate p73 transcriptionally and posttranslationally, increasing mRNA levels and protein stability.
    • Found that p73(-/-) cells and cells with p73 inhibition are more resistant to stress-induced apoptosis, indicating p73's pro-apoptotic role.

    Conclusions:

    • Several stress signals can activate p73 in vivo.
    • p73 plays a significant role in mediating apoptosis in response to diverse cellular stresses.
    • Targeting p73 activation with stress-inducing agents presents a potential therapeutic avenue for cancers with intact p73.