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Updated: May 5, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
Effects of fibronectin and type IV collagen on osteosarcoma cell apoptosis
Zerrin Incesu1, Ibrahim Hatipoğlu, Hülya Sivas
1Department of Biochemistry, Faculty of Farmacy, Anadolu University, Eskişehir, Turkey. zseller@anadolu.edu.tr
Abstract:
The aims of this study are the investigation of the effects of fibronectin and type IV collagen extracellular matrix proteins and the role of caspase-3 and -9 on cis-platin induced U2-OS apoptosis were studied. First the cytotoxic effects of cis-platin on cell system were investigated by colorimetric method and than morphological and ELISA analysis were used for determination of cell apoptosis when induced with cis-platin. In addition, after adhering the cells to fibronection or type IV collagen proteins, the apoptotic rate and the effects of caspase-3 and -9 were also investigated by ELISA in presence of specific inhibitors. U2-OS cells showed 20% cytotoxicity after treatment with 2.4 microM of cis-platin for 48 h. Morphological and the numerical data showed that cis-platin was able to induced apoptosis on cells as a dose-dependent manner. Caspase-3 and -9 inhibitors inhibited cis-platin-induced apoptosis in U2-OS cells, respectively. The binding of cells to 10 microg/mL of fibronectin but not type IV collagen enhanced the apoptosis about 2.5 fold that effects inhibited with caspase-3 inhibitor. The caspase-3 and -9 are involved in the apoptotic signals induced by cis-platin in U2-OS. The binding to fibronectin, but not type IV collagen enhanced the apoptotic response of U2-OS and fibronectin-dependent apoptosis was activated by caspase-3. These finding might be useful for patients to fight against osteosarcoma.
Insights
Cis-platin induces apoptosis in U2-OS cells, with fibronectin enhancing this effect via caspase-3 activation. These findings offer insights into fighting osteosarcoma.
Area of Science:
- Cell biology
- Molecular oncology
Background:
- Osteosarcoma is a significant bone cancer.
- Understanding cis-platin's apoptotic mechanisms is crucial for treatment.
- Extracellular matrix proteins may influence drug response.
Purpose of the Study:
- Investigate cis-platin-induced apoptosis in U2-OS cells.
- Determine the role of fibronectin and type IV collagen in this process.
- Elucidate the involvement of caspase-3 and caspase-9.
Main Methods:
- Colorimetric assays for cytotoxicity.
- Morphological and ELISA analysis for apoptosis.
- ELISA with specific inhibitors to study caspase roles and protein interactions.
Main Results:
- Cis-platin induced dose-dependent apoptosis in U2-OS cells.
- Caspase-3 and caspase-9 inhibitors reduced cis-platin-induced apoptosis.
- Fibronectin, but not type IV collagen, enhanced apoptosis 2.5-fold.
- Fibronectin-enhanced apoptosis was inhibited by caspase-3 inhibitors.
Conclusions:
- Cis-platin effectively induces apoptosis in U2-OS cells.
- Caspase-3 and caspase-9 are key mediators of cis-platin-induced apoptosis.
- Fibronectin enhances cis-platin-induced apoptosis through caspase-3 activation, suggesting a potential therapeutic target for osteosarcoma.
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