Related Experiment Video
Updated: Apr 24, 2026

Assessment of Ovarian Cancer Spheroid Attachment and Invasion of Mesothelial Cells in Real Time
Published on: May 20, 2014
Microarray-based detection and expression analysis of extracellular matrix proteins in drug‑resistant ovarian cancer
Radosław Januchowski1, Piotr Zawierucha1, Marcin Ruciński1
1Department of Histology and Embryology, Poznań University of Medical Sciences, Poznań 61‑781, Poland.
Abstract:
Ovarian cancer is the most lethal gynecological malignancy. Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular matrix (ECM) can influence drug resistance by inhibiting the penetration of the drug into cancer tissue as well as increased apoptosis resistance. In the present study, we report changes in the ECM and related gene expression pattern in methotrexate-, cisplatin-, doxorubicin-, vincristine-, topotecan- and paclitaxel-resistant variants of the W1 ovarian cancer cell line. The resistant variants of the W1 cell line were generated by stepwise selection of cells with an increasing concentration of the indicated drugs. Affymetrix GeneChip® Human Genome U219 Array Strips were used for hybridizations. Independent t-tests were used to determinate the statistical significance of results. Genes whose expression levels were higher than the assumed threshold (upregulated, >5-fold and downregulated, <5-fold) were visualized using the scatter plot method, selected and listed in the tables. Among the investigated genes, expression of 24 genes increased, expression of 14 genes decreased and expression of three genes increased or decreased depending on the cell line. Among the increased genes, expression of 10 increased very significantly, >20-fold. These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6. The expression of seven genes decreased very significantly: ITGA1, COL1A2, LAMA2, GPC3, KRT23, VIT and HMCN1. The expression pattern of ECM and related genes provided the preliminary view into the role of ECM components in cytostatic drug resistance of cancer cells. The exact role of the investigated genes in drug resistance requires further investigation.
Insights
This study investigated changes in extracellular matrix (ECM) gene expression in ovarian cancer cells resistant to chemotherapy. Key ECM genes were identified, offering insights into drug resistance mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer is a highly lethal gynecological malignancy.
- Development of multiple drug resistance (MDR) is a major cause of chemotherapy failure.
- Extracellular matrix (ECM) components may influence drug resistance by affecting drug penetration and apoptosis resistance.
Purpose of the Study:
- To investigate changes in the expression patterns of extracellular matrix (ECM) and related genes in drug-resistant ovarian cancer cell lines.
- To identify candidate genes involved in mediating resistance to cytostatic drugs.
Main Methods:
- Generation of drug-resistant W1 ovarian cancer cell line variants through stepwise selection.
- Microarray analysis using Affymetrix GeneChip® Human Genome U219 Array Strips to assess gene expression.
- Statistical analysis using independent t-tests and visualization of gene expression changes.
Main Results:
- Significant alterations in the expression of 24 increased and 14 decreased ECM-related genes were observed.
- Ten genes showed very significant upregulation (>20-fold), including ITGB1BP3, COL3A1, and TGFBI.
- Seven genes exhibited very significant downregulation, including ITGA1, COL1A2, and LAMA2.
Conclusions:
- The study provides a preliminary overview of ECM gene expression patterns in drug-resistant ovarian cancer cells.
- Identified ECM genes may play a role in the development of cytostatic drug resistance.
- Further research is needed to elucidate the precise function of these genes in drug resistance.

