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Silibinin Triggers Mitochondrial Apoptosis and Declines Clonogenic Potential in Detroit 562 Human Pharyngeal
Serban Talpos1, Doina Chioran2, George Cătălin Alexandru3,4
1Discipline of Oral and Maxillo-Facial Surgery, Faculty of Dental Medicine, "Victor Babes" University of Medicine and Pharmacy Timisoara, Revolutiei Boulevard 9, 300041 Timisoara, Romania.
Abstract:
Background and Objectives: Oropharyngeal squamous cell carcinoma (OPSCC) is a common type of head and neck cancer with a progressive incidence in recent years. The limitations and the side effects associated with the current treatments require new therapeutic alternatives. Silibinin (SIL) is a phytocompound with multifaceted properties that has demonstrated antitumor effects in several types of cancer. The aim of this study was to assess the potential anticancer effects of SIL in Detroit 562 human pharyngeal cancer cells, an ideal model for HPV-negative OPSCC. Materials and Methods: Detroit 562 cells and HGF-1- human gingival fibroblasts were used as experimental models. For the mechanistic investigations, different methods, such as MTT assay, bright field microscopy, immunofluorescence staining, and specific assays and kits were applied to quantify intracellular ROS production, activation of caspases, and the colony formation assay. Results: Treatment with SIL (25-200 µM) for 48 h induced a selective cytotoxic effect in Detroit 562 cancer cells, being minimally toxic to healthy cells. The cytotoxic mechanism of action was characterized by a decreased cell viability, morphological alterations, elevation of intracellular ROS, decreased mitochondrial potential, mitochondrial and nuclear dysmorphologies, activation of caspases 9 and 3/7 and apoptosis occurrence, and decreased long-term colony formation. Conclusions: These findings show that SIL could represent a potential alternative therapy for HPV-negative OPSCC by triggering mitochondrial apoptosis and exerting a decline in the colonogenicity of Detroit 562 cancer cells.
Insights
Silibinin (SIL) shows anticancer effects against human pharyngeal cancer cells. This phytocompound selectively kills cancer cells by inducing apoptosis and reducing colony formation, offering a potential therapy for HPV-negative oropharyngeal squamous cell carcinoma (OPSCC).
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Oropharyngeal squamous cell carcinoma (OPSCC) incidence is rising, necessitating novel therapeutic strategies due to current treatment limitations.
- Silibinin (SIL), a plant-derived compound, exhibits promising antitumor properties across various cancer types.
- HPV-negative OPSCC requires alternative treatments, making Detroit 562 cells a relevant model for investigation.
Purpose of the Study:
- To evaluate the anticancer potential of Silibinin (SIL) in Detroit 562 human pharyngeal cancer cells.
- To investigate the specific mechanisms underlying SIL's cytotoxic effects in HPV-negative OPSCC models.
Main Methods:
- Cell viability assessed using MTT assay.
- Microscopy, immunofluorescence, and specific kits used to analyze ROS production, mitochondrial potential, and caspase activation.
- Colony formation assays evaluated long-term cancer cell proliferation.
Main Results:
- Silibinin (25-200 µM) demonstrated selective cytotoxicity against Detroit 562 cancer cells with minimal toxicity to healthy cells.
- SIL treatment induced apoptosis via caspase activation, increased intracellular ROS, and altered mitochondrial morphology.
- Reduced cell viability, nuclear abnormalities, and decreased colony formation were observed.
Conclusions:
- Silibinin effectively triggers mitochondrial apoptosis in HPV-negative OPSCC cells.
- SIL reduces the colonogenicity of Detroit 562 cancer cells, indicating its potential as an alternative therapy.
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