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CAR is a cell-cell adhesion protein in human cancer cells and is expressionally modulated by dexamethasone, TNFalpha,

A Brüning1, I B Runnebaum

  • 1Department of Obstetrics and Gynecology, Molecular Biology Laboratory, University of Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany.

Gene Therapy
|February 7, 2003
PubMed

Insights

Dexamethasone reduces adenoviral gene transfer by downregulating the coxsackie adenovirus receptor (CAR). Tumor necrosis factor-alpha and transforming growth factor-beta also impact CAR expression and adenoviral delivery efficiency.

Area of Science:

  • Molecular Biology
  • Gene Therapy
  • Cell Biology

Background:

  • The coxsackie adenovirus receptor (CAR) is vital for adenoviral vector entry in gene therapy.
  • Dexamethasone is used in clinical trials to mitigate adenoviral vector side effects.

Purpose of the Study:

  • To investigate the impact of dexamethasone, TNF-alpha, and TGF-beta on adenoviral gene transfer.
  • To explore the role of CAR and integrins in adenoviral vector efficiency.

Main Methods:

  • Adenoviral vectors (AdGal, p53-expressing) were used to assess gene transfer in human cancer cell lines.
  • Quantitative analysis of CAR and integrin expression via transcriptional downregulation.
  • Confocal immunofluorescence microscopy to determine CAR localization.

Main Results:

  • Dexamethasone decreased adenoviral gene transfer and downregulated CAR and integrin alpha5beta1 expression.
  • TNF-alpha differentially affected CAR expression but increased adenovirus-binding integrins, enhancing gene transfer.
  • TGF-beta reduced CAR expression and adenoviral gene transfer in ovarian cancer cells.

Conclusions:

  • Cell adhesion, dexamethasone, TNF-alpha, and TGF-beta can modulate adenoviral gene delivery efficiency.
  • Understanding these factors is crucial for optimizing clinical cancer gene therapy strategies.

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