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Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells
Dae-Hee Lee1, Dong-Wook Kim2, Chang-Hwa Jung3
1Departments of Surgery and Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Abstract:
Glioblastoma multiforme (GBM) is the most lethal and aggressive astrocytoma of primary brain tumors in adults. Although there are many clinical trials to induce the cell death of glioblastoma cells, most glioblastoma cells have been reported to be resistant to TRAIL-induced apoptosis. Here, we showed that gingerol as a major component of ginger can induce TRAIL-mediated apoptosis of glioblastoma. Gingerol increased death receptor (DR) 5 levels in a p53-dependent manner. Furthermore, gingerol decreased the expression level of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and increased pro-apoptotic protein, Bax and truncate Bid, by generating reactive oxygen species (ROS). We also found that the sensitizing effects of gingerol in TRAIL-induced cell death were blocked by scavenging ROS or overexpressing anti-apoptotic protein (Bcl-2). Therefore, we showed the functions of gingerol as a sensitizing agent to induce cell death of TRAIL-resistant glioblastoma cells. This study gives rise to the possibility of applying gingerol as an anti-tumor agent that can be used for the purpose of combination treatment with TRAIL in TRAIL-resistant glioblastoma tumor therapy.
Insights
Gingerol, a ginger component, combats TRAIL-resistant glioblastoma by increasing death receptors and generating reactive oxygen species. This sensitizes cancer cells to TRAIL-induced apoptosis, offering a potential combination therapy for glioblastoma multiforme.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Glioblastoma multiforme (GBM) is an aggressive brain tumor resistant to standard therapies.
- TRAIL-induced apoptosis is often ineffective in GBM cells due to resistance mechanisms.
Purpose of the Study:
- To investigate gingerol's potential to sensitize TRAIL-resistant glioblastoma cells to apoptosis.
- To elucidate the molecular mechanisms underlying gingerol's sensitizing effects.
Main Methods:
- Assessing gingerol's effect on death receptor (DR) 5 levels and p53 dependency.
- Quantifying changes in pro-apoptotic and anti-apoptotic protein expression.
- Evaluating the role of reactive oxygen species (ROS) and Bcl-2 in gingerol's action.
Main Results:
- Gingerol upregulated DR5 in a p53-dependent manner.
- Gingerol decreased anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, XIAP) and increased pro-apoptotic proteins (Bax, tBid) via ROS generation.
- ROS scavenging or Bcl-2 overexpression blocked gingerol's sensitizing effect on TRAIL-induced cell death.
Conclusions:
- Gingerol acts as a sensitizing agent, enhancing TRAIL-induced apoptosis in resistant glioblastoma cells.
- Gingerol's mechanism involves ROS generation, modulation of apoptosis-related proteins, and p53 pathway activation.
- Gingerol shows promise as a combination therapy agent for glioblastoma treatment.
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