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Updated: Aug 11, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
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.
Abstract:
The coxsackie and adenovirus receptor (CAR) is a key factor in adenoviral cancer gene therapy. Reduced expression of CAR during progression of prostate and bladder cancer has been reported. In embryonic development and tissue differentiation, CAR is also differentially expressed. This study suggests a role of CAR expression in cell adhesion and cell motility of human cancer cells. Stable CAR-expressing clones from E-cadherin-deficient A2780 ovarian and CaSki cervical cancer cells with originally low and high CAR expression levels, respectively, were established. CAR reexpression in otherwise singularly growing A2780 parental cells resulted in formation of cell-cell contacts and aggregation in cell clusters. CAR overexpression in cell adhesion-forming CaSki cells did not result in morphological changes. Migration of the A2780 CAR clones was strongly reduced as characterized by using spread-off assays. Using migration chambers, formation of satellite colonies was reduced by 97% in CAR-expressing A2780 cell clones and by 23% in CAR-expressing CaSki cell clones. Parental A2780 and CaSki cells selected for high migratory ability by using migration chambers expressed endogenous CAR on lower levels associated with lower adenoviral transduction efficiency. Our data suggest CAR as a new inhibitory factor for cancer cell migration.
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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