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Migratory, invasive and metastatic capacity of NCAM transfected rat glioma cells
K Edvardsen1, N Brünner, M Spang-Thomsen
1Research Centre for Medical Biotechnology, University of Copenhagen, Panum Institute, Denmark.
Abstract:
A cDNA encoding a transmembrane 140 kDa isoform of the neural cell adhesion molecule, NCAM, was transfected into the rat glioma cell line BT4Cn. Transfectants with a homogeneously high expression of NCAM-B showed a decreased capacity for penetration of an artificial basement membrane when compared to cells transfected with expression-vector alone or untransfected cells. However, when injected subcutaneously into nude mice, both NCAM expressing cells and control cells produced invasive tumors. Nude mice injected with NCAM positive cells developed tumors with slower growth rates as compared to those induced by NCAM negative cells. This implies that NCAM may not only be involved in adhesive and motile behaviour of glioma cells, but also in their growth regulation.
Insights
High expression of neural cell adhesion molecule (NCAM) in glioma cells reduced their ability to penetrate barriers but did not prevent tumor formation. NCAM expression also slowed tumor growth in mice.
Area of Science:
- Neuroscience
- Cell Biology
- Cancer Research
Background:
- Neural cell adhesion molecule (NCAM) plays roles in cell adhesion and migration.
- Glioma is a primary brain tumor with significant morbidity and mortality.
- Understanding NCAM's role in glioma progression is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the functional role of a specific NCAM isoform (NCAM-B) in glioma cell behavior.
- To determine NCAM's impact on glioma cell invasiveness and tumor growth in vivo.
Main Methods:
- Transfection of rat glioma cells (BT4Cn) with NCAM-B cDNA.
- In vitro assessment of cell penetration through an artificial basement membrane.
- Subcutaneous tumor induction in nude mice to evaluate in vivo tumor growth and invasiveness.
Main Results:
- NCAM-B expressing glioma cells exhibited reduced capacity to penetrate artificial basement membranes in vitro.
- Both NCAM-expressing and control cells formed invasive tumors when injected into nude mice.
- Tumors derived from NCAM-positive cells showed slower growth rates compared to NCAM-negative tumors.
Conclusions:
- NCAM-B expression influences glioma cell invasiveness, decreasing penetration through extracellular matrix barriers.
- NCAM is implicated not only in glioma cell adhesion and motility but also in regulating tumor growth rate.
- Targeting NCAM may offer a dual therapeutic strategy for glioma by affecting both invasion and proliferation.