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Published on: March 28, 2021
Inhibitory effect of triptolide on glioblastoma multiforme in vitro
1College of Life Science and Biotechnology, Jiaotong University, Shanghai, People's Republic of China. jianlinmt@163.com
Abstract:
This study investigated the effect of triptolide, derived from the traditional Chinese herb Tripterygium wilfordii, on the growth of glioblastoma multiforme (GBM) cells. Glioma cell lines U251MG and U87MG and normal human fetal astrocytes were exposed to various concentrations of triptolide, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium and colony formation assays were used to measure cell growth and survival. Cell apoptosis was determined using annexin V. Levels of the oncogenic transformation-related proteins Ras-guanosine triphosphate (Ras-GTP), extracellular signal-regulated kinase (ERK) and Akt were determined by Western blotting. Triptolide caused a dose-dependent decrease in proliferation and increase in apoptosis in the glioma cell lines. Since U87MG has a wildtype p53 gene while U251MG harbours a mutated p53 gene, these results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway. Treatment of GBM cells with triptolide attenuated both the Ras/ERK and the Ras/Akt signalling pathways. This could provide a theoretical basis for triptolide treatment in GBM, but further animal studies and clinical research are necessary.
Insights
Triptolide, from Tripterygium wilfordii, inhibits glioblastoma multiforme (GBM) growth and induces apoptosis through a p53-independent pathway, impacting Ras/ERK and Ras/Akt signaling.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Glioblastoma multiforme (GBM) is an aggressive brain tumor with limited treatment options.
- Triptolide, a compound from Tripterygium wilfordii, has shown potential anti-cancer properties.
- Understanding triptolide's mechanism in GBM is crucial for developing new therapies.
Purpose of the Study:
- To investigate the anti-proliferative and pro-apoptotic effects of triptolide on glioblastoma multiforme (GBM) cells.
- To elucidate the signaling pathways affected by triptolide in GBM.
- To determine if triptolide's action is dependent on the p53 gene status.
Main Methods:
- Exposure of U251MG and U87MG glioblastoma cell lines to varying triptolide concentrations.
- Cell proliferation and survival assessed using MTT and colony formation assays.
- Apoptosis analysis via annexin V staining.
- Western blotting to measure levels of Ras-GTP, ERK, and Akt proteins.
Main Results:
- Triptolide demonstrated a dose-dependent reduction in GBM cell proliferation and survival.
- Triptolide significantly increased apoptosis in both wildtype p53 (U87MG) and mutated p53 (U251MG) glioblastoma cells, indicating a p53-independent mechanism.
- Triptolide treatment attenuated the Ras/ERK and Ras/Akt signaling pathways in GBM cells.
Conclusions:
- Triptolide exhibits potent anti-glioblastoma activity by inducing apoptosis via a p53-independent pathway.
- The observed effects are linked to the modulation of Ras/ERK and Ras/Akt signaling cascades.
- Triptolide presents a potential therapeutic agent for GBM, warranting further preclinical and clinical investigation.
