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The ability in adhesion and invasion of drug-resistant human glioma cells
Abstract:
Drug-resistance is critical in treating malignant tumors, and a variety of treatments are given to control it. Little study has been done, however, on biological changes in tumor cell activity in the course of acquiring drug-resistance. We used a glioma cell line to study changes in cell adhesion and invasion on acquiring drug-resistance. Human glioma culture cell line IN157 was used to establish the cell lines resistant to etoposide (VP-16), vincristine sulfate (VCR), and doxorubicin hydrochloride (DOX). Expressions of integrin alpha2, alpha3, alpha5, and beta1, neuronal cell adhesion molecule (NCAM), and matrix metalloproteinases (MMPs) were examined by flow cytometry. In drug-resistant cells, integrin expression was enhanced and NCAM expression was reduced. Adhesions to the extracellar matrix (ECM) proteins (laminin, fibronectin or type IV collagen) were studied. The adhesive ability of all cell lines increased in a concentration-dependent manner. Adhesion of drug-resistant cells was significantly stronger than that of IN157. The cell invasion of drug-resistant cell lines to the basal membrane was significantly lower than that of IN157. The cell invasion of IN157 was significantly suppressed by adding anti-NCAM antibody. In the case of IN157 with the acquisition of drug-resistance, an increase in the expression of integrins may have enhanced the adhesion to ECM proteins. This finding may be concerned with the decreased activity of drug-resistant cell lines in invading the basement membrane. NCAM expression in drug-resistant cell lines was reduced and anti-NCAM antibody abated invasion of IN157, suggesting that NCAM is involved in IN157 invasion.
Insights
Drug resistance in glioma cells alters cell adhesion and invasion. Resistant cells show increased integrin expression, enhanced extracellular matrix adhesion, and reduced invasion, with NCAM playing a key role.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Drug resistance is a major challenge in malignant tumor treatment.
- Biological changes in tumor cells during drug resistance acquisition are not well understood.
- Investigating these changes is crucial for developing effective cancer therapies.
Purpose of the Study:
- To investigate biological changes in cell adhesion and invasion in a drug-resistant glioma cell line.
- To examine the expression of specific cell adhesion molecules and matrix metalloproteinases.
- To understand the role of these molecules in the development of drug resistance.
Main Methods:
- Established drug-resistant human glioma cell lines (IN157) against etoposide, vincristine, and doxorubicin.
- Analyzed expression of integrins (alpha2, alpha3, alpha5, beta1), NCAM, and MMPs using flow cytometry.
- Assessed cell adhesion to extracellular matrix proteins and cell invasion through a basal membrane model.
Main Results:
- Drug-resistant cells exhibited enhanced integrin expression and reduced NCAM expression compared to parental cells.
- Adhesion to extracellular matrix proteins (laminin, fibronectin, type IV collagen) was significantly stronger in drug-resistant cells.
- Drug-resistant cells showed significantly lower invasion capacity, and anti-NCAM antibody suppressed invasion in parental cells.
Conclusions:
- Increased integrin expression in drug-resistant glioma cells enhances their adhesion to the extracellular matrix.
- Reduced NCAM expression in resistant cells correlates with decreased invasion, suggesting NCAM's role in glioma cell invasion.
- These findings provide insights into the molecular mechanisms underlying drug resistance and invasion in glioma.
