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Influence of silibinin and β-β-dimethylacrylshikonin on chordoma cells
Zohreh Jahanafrooz1, Alexander Stallinger2, Ines Anders2
1Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Biotechnology, Higher Education Institute of Rab-Rashid, Tabriz, Iran.
Background:
Chordoma, slow growing bone tumours originating from remnants of the notochord, leave affected patients with a median survival of six years. The high recurrence rate of chordoma, together with limited treatment options and bad overall prognosis, make the development of new treatment options urgently necessary.
Purpose:
In this study, the potential of two natural products, silibinin and β-β-dimethylacrylshikonin (DMAS), was tested on clival (MUG-CC1 and UM-Chor1) as well as sacral (MUG-Chor1 and U-CH2) chordoma cell lines. The treatment was administered both as single- and combined therapy.
Methods:
For investigation of cell viability, the Cell Titer 96 Aqueous Non-Radioactive Cell Proliferation Assay Kit was used. Apoptosis induction was studied by flow cytometry, (Annexin V/SYTOX Green, caspase-3) and RT-qPCR. Pathway analyses were performed by western blot.
Results:
Both drugs were found to reduce cell viability alone as well as in combination in a dose dependent manner, with DMAS being more efficient than silibinin. The mode of cell death was mainly apoptosis in DMAS treated samples, while the combination therapy led to apoptosis as well as late-apoptosis/necrosis. Silibinin therapy alone, although reducing cell viability, did not lead to significant apoptotic effects in the performed assays. Focussing on the molecular mechanism of DMAS induced apoptosis, it was found that major genes of the mitochondrial apoptosis pathway, like NOXA and PUMA were overexpressed. Additionally, western blot experiments showed a decrease of ERK/pERK, STAT3/pSTAT3 (Tyr705) and AKT/pAKT expression/activation levels under DMAS treatment.
Conclusion:
DMAS is a promising new candidate for chordoma therapy, while silibinin or a combination of both is less favourable.
Insights
The natural compound β-β-dimethylacrylshikonin (DMAS) shows promise in treating chordoma bone tumors by inducing apoptosis. Silibinin alone or in combination was less effective than DMAS for chordoma therapy.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Chordoma is a slow-growing bone tumor with a poor prognosis and limited treatment options.
- The median survival for chordoma patients is only six years, necessitating novel therapeutic strategies.
Purpose of the Study:
- To evaluate the anti-cancer potential of two natural products, silibinin and β-β-dimethylacrylshikonin (DMAS), against chordoma cell lines.
- To investigate the efficacy of single-agent and combination therapies using silibinin and DMAS in chordoma treatment.
Main Methods:
- Chordoma cell viability was assessed using the Cell Titer 96 Aqueous Non-Radioactive Cell Proliferation Assay.
- Apoptosis induction was analyzed via flow cytometry (Annexin V/SYTOX Green, caspase-3) and RT-qPCR.
- Molecular mechanisms were explored through western blot analysis and pathway investigations.
Main Results:
- Both silibinin and DMAS reduced chordoma cell viability in a dose-dependent manner, with DMAS exhibiting greater efficacy.
- DMAS primarily induced apoptosis, while combination therapy resulted in apoptosis and late-apoptosis/necrosis.
- DMAS treatment upregulated key apoptosis genes (NOXA, PUMA) and downregulated signaling pathways (ERK, STAT3, AKT).
Conclusions:
- β-β-dimethylacrylshikonin (DMAS) demonstrates significant potential as a novel therapeutic agent for chordoma.
- Silibinin, alone or in combination with DMAS, showed less favorable outcomes compared to DMAS monotherapy.
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