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Published on: December 8, 2015
Enhancement of Fas-ligand-mediated programmed cell death by taurolidine
Ruediger Stendel1, Louis Scheurer, Gisela Stoltenburg-Didinger
1Department of Neurosurgery, Benjamin Franklin Medical Center, Free University of Berlin Hindenburgdamm 30, 12203 Berlin, Germany. r.stendel@web.de
Background:
Taurolidine was recently found to have a direct and selective antineoplastic effect on brain tumor cells. The ability of taurolidine to exert antineoplastic action by enhancement of Fas-mediated apoptosis in different malignant glioma cell lines was investigated.
Materials And Methods:
Human derived U373 cells were cultured and incubated with taurolidine and the median inhibitory concentration (IC50) was calculated. Flow cytometric analysis was performed to assess changes in DNA content. The cells were qualitatively and quantitatively examined using light microscopy and electron microscopy. LN-18 and LN-229 cells were incubated in the absence or presence of either Fas-ligand, taurolidine or respective combinations thereof. The cell viability was determined by adding a double concentrated WST-1 reagent. The activity of the mitochondrial succinate reductase was measured in an ELISA reader.
Results:
The exposure of U373 cells to taurolidine led to a concentration-dependent (IC50 35.8 +/- 2.2 micrograms/ml) loss of cell viability. Flow cytometric analysis demonstrated a concentration-dependent appearance of DNA debris in the sub-Go/G1 region. In the presence of 6.25 vol.% Fas-ligand, LN-18 cells displayed more than 90% loss of cell viability, whereas the viability of LN-229 cells was reduced only at higher concentrations of Fas-ligand. Taurolidine by itself did not appreciably affect the viability of LN-18 cells in the investigated concentration range, but was able to enhance the effect of Fasligand on LN-18 cells. The exposure of LN-229 cells to taurolidine alone caused an appreciable loss of cell viability by about 70% at the highest concentration tested. Cell destruction by Fas-ligand (10 vol.%) was enhanced in the presence of taurolidine.
Conclusion:
The antineoplastic activity of taurolidine seems to be partially based on the enhancement of Fas-ligand-induced apoptosis. In addition, taurolidine was demonstrated to have an antieoplastic effect independent of Fas-ligand. Perhaps taurolidine exerts antineoplastic activity based on different mechanisms.
Insights
Taurolidine shows direct anti-cancer effects on brain tumor cells by enhancing Fas-mediated apoptosis. It also exhibits independent anti-cancer activity, suggesting multiple mechanisms of action against malignant glioma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Taurolidine exhibits direct antineoplastic effects on brain tumor cells.
- Investigated taurolidine's role in enhancing Fas-mediated apoptosis in malignant glioma.
Purpose of the Study:
- To investigate the mechanism of taurolidine's antineoplastic action.
- To determine if taurolidine enhances Fas-mediated apoptosis in glioma cells.
Main Methods:
- U373 cells treated with taurolidine to determine IC50 and DNA content via flow cytometry.
- LN-18 and LN-229 cells treated with Fas-ligand and/or taurolidine.
- Cell viability assessed using WST-1 reagent; mitochondrial succinate reductase activity measured.
Main Results:
- Taurolidine induced concentration-dependent cell death in U373 cells (IC50 35.8 µg/ml) and DNA fragmentation.
- Taurolidine enhanced Fas-ligand-induced apoptosis in LN-18 cells (>90% viability loss).
- Taurolidine showed independent cytotoxic effects on LN-229 cells (70% viability loss at highest concentration).
Conclusions:
- Taurolidine's antineoplastic activity is partly mediated by enhancing Fas-ligand-induced apoptosis.
- Taurolidine demonstrates an independent antineoplastic effect, suggesting multiple mechanisms.
- Further research into taurolidine's diverse mechanisms against brain tumors is warranted.
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