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Updated: May 4, 2026

Tumor Treating Field Therapy in Combination with Bevacizumab for the Treatment of Recurrent Glioblastoma
Published on: October 27, 2014
Quercetin and sorafenib as a novel and effective couple in programmed cell death induction in human gliomas
Joanna Jakubowicz-Gil1, Ewa Langner, Dorota Bądziul
1Department of Comparative Anatomy and Anthropology, Maria Curie-Skłodowska University, Akademicka 19, 20-033, Lublin, Poland, jjgil@poczta.umcs.lublin.pl.
Abstract:
The aim of the present study was to investigate the effect of sorafenib and quercetin on the induction of apoptosis and autophagy in human anaplastic astrocytoma (MOGGCCM) and glioblastoma multiforme (T98G) cell lines. In MOGGCCM cells, sorafenib initiated mainly apoptosis, mediated by the mitochondrial pathway with mitochondrial membrane permeabilization, cytochrome c release to the cytoplasm, and activation of caspase 9 and 3. Additional incubation with quercetin potentiated the pro-apoptotic properties of sorafenib. In T98G cells, autophagy was observed most frequently after the sorafenib treatment. It was accompanied by increased beclin 1 and LC3II expression. Administration of quercetin after the sorafenib treatment resulted in an increased number of autophagic cells. After simultaneous drug application, the level of autophagy was lower in favour of apoptosis. Inhibition of heat shock proteins expression by specific small interfering RNA significantly increased the sensitivity of both the cell lines to induction of apoptosis, but not autophagy. We demonstrated for the first time that sorafenib and quercetin are very effective programmed cell death inducers in T98G and MOGGCCM cells, especially in cells with blocked expression of heat shock proteins.
Insights
Sorafenib and quercetin effectively induce programmed cell death in glioblastoma and anaplastic astrocytoma cells. Inhibiting heat shock proteins enhances this effect, offering a promising therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Glioblastoma multiforme (T98G) and anaplastic astrocytoma (MOGGCCM) are aggressive brain tumors.
- Understanding cell death pathways like apoptosis and autophagy is crucial for developing new cancer therapies.
Purpose of the Study:
- To investigate the effects of sorafenib and quercetin on apoptosis and autophagy in MOGGCCM and T98G cell lines.
- To explore the combined effects of these drugs and the role of heat shock proteins.
Main Methods:
- Treatment of MOGGCCM and T98G cells with sorafenib and quercetin.
- Analysis of apoptosis via mitochondrial pathway markers (caspase 9, 3) and cytochrome c release.
- Assessment of autophagy through beclin 1 and LC3II expression.
- Utilizing small interfering RNA to inhibit heat shock proteins.
Main Results:
- Sorafenib induced apoptosis in MOGGCCM cells and autophagy in T98G cells.
- Quercetin potentiated sorafenib's pro-apoptotic effects and increased autophagy when administered sequentially.
- Simultaneous drug application favored apoptosis over autophagy.
- Inhibition of heat shock proteins significantly enhanced apoptosis induction in both cell lines.
Conclusions:
- Sorafenib and quercetin are potent inducers of programmed cell death in MOGGCCM and T98G cells.
- Combined treatment, especially with heat shock protein inhibition, shows significant potential for glioblastoma therapy.
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