The coxsackie adenovirus receptor inhibits cancer cell migration

Ansgar Brüning1, Ingo B Runnebaum

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

Insights

The coxsackie and adenovirus receptor (CAR) inhibits cancer cell migration. Re-expressing CAR in ovarian and cervical cancer cells reduced their ability to move, suggesting CAR

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The coxsackie and adenovirus receptor (CAR) is crucial for adenoviral cancer gene therapy.
  • Reduced CAR expression is observed in advanced prostate and bladder cancers.
  • CAR expression is also differential during embryonic development and tissue differentiation.

Purpose of the Study:

  • To investigate the role of CAR expression in the cell adhesion and motility of human cancer cells.
  • To establish stable CAR-expressing clones from E-cadherin-deficient A2780 ovarian and CaSki cervical cancer cells.
  • To analyze the impact of CAR re-expression on cell-cell contacts, aggregation, and migration.

Main Methods:

  • Generation of stable CAR-expressing clones from A2780 and CaSki cancer cell lines.
  • Assessment of cell-cell contacts and aggregation.
  • Evaluation of cell migration using spread-off assays and migration chambers.
  • Analysis of endogenous CAR levels in high-migratory cancer cell populations.

Main Results:

  • CAR re-expression in A2780 cells induced cell-cell contacts and aggregation.
  • CAR overexpression in CaSki cells did not cause significant morphological changes.
  • Migration was significantly reduced in CAR-expressing A2780 clones (97%) and CaSki clones (23%).
  • Highly migratory parental cells showed lower endogenous CAR levels and reduced adenoviral transduction efficiency.

Conclusions:

  • CAR expression plays a role in regulating cancer cell adhesion and motility.
  • CAR re-expression inhibits cancer cell migration, particularly in E-cadherin-deficient cells.
  • CAR may function as a novel inhibitory factor for cancer cell migration.

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