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Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases
14:57

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Published on: October 10, 2020

p63 regulates glutaminase 2 expression.

Arianna Giacobbe1, Lucilla Bongiorno-Borbone, Francesca Bernassola

  • 1Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy.

Cell Cycle (Georgetown, Tex.)
|April 12, 2013
PubMed
Summary
This summary is machine-generated.

The TAp63 transcription factor regulates cell metabolism by inducing the GLS2 gene. This TAp63-GLS2 pathway is crucial for epidermal differentiation and acts as an antioxidant pathway in cancer cells.

Keywords:
colon carcinomaglutaminolysisp63skin differentiation

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Area of Science:

  • Molecular Biology
  • Cell Metabolism
  • Cancer Biology

Background:

  • The transcription factor p63 is essential for epidermal development and tumorigenesis.
  • p63 isoforms, particularly TAp63, play roles in cellular processes beyond their established functions.

Purpose of the Study:

  • To investigate the role of TAp63 isoforms in regulating cell metabolism.
  • To identify target genes of TAp63 involved in metabolic regulation.
  • To explore the function of the TAp63-GLS2 axis in epidermal differentiation and cancer.

Main Methods:

  • Chromatin immunoprecipitation (ChIP) assays to confirm TAp63 binding to the GLS2 promoter.
  • Luciferase reporter assays to assess TAp63-mediated transcriptional activity.
  • siRNA-mediated gene depletion to evaluate the functional impact of GLS2.
  • In vitro differentiation models of primary human keratinocytes.
  • Analysis of GLS2 and TAp63 expression in cancer cell lines and patient samples.

Main Results:

  • TAp63 directly binds to the GLS2 promoter and induces its expression, regulating cell metabolism.
  • GLS2 and TAp63 expression increase during keratinocyte differentiation, and GLS2 depletion impairs this process.
  • The TAp63/GLS2 axis is upregulated under oxidative stress in cancer cells.
  • GLS2 depletion sensitizes cancer cells to ROS-induced apoptosis, highlighting its role as an antioxidant pathway.
  • GLS2 is upregulated in colon adenocarcinoma, suggesting pathological relevance.

Conclusions:

  • GLS2 is a direct transcriptional target of TAp63.
  • The TAp63-GLS2 pathway is critical for epidermal differentiation and cellular antioxidant defense.
  • This axis plays significant roles in both normal physiological processes and pathological conditions like cancer.