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Okanin Inhibits Cell Growth and Induces Apoptosis and Pyroptosis in Oral Cancer
Wei-Tso Chia1,2,3, Kuei-Yuan Chen4,5, Cheng-Yu Yang4,5
1Department of Orthopedics, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu 302, Taiwan.
Background:
Okanin, a flavonoid compound derived from Bidens pilosa L., has garnered attention for its anti-inflammatory properties. Although Bidens pilosa is commonly used in healthcare products and functional foods, the anticancer potential of okanin, particularly in oral cancer, remains underexplored. This study aims to investigate the effects of okanin on oral cancer cell lines and its potential as a therapeutic agent.
Methods:
The study involved assessing the cytotoxic effects of okanin on oral cancer cell lines SAS, SCC25, HSC3, and OEC-M1. The IC50 values were determined using methylene blue assays, and the clonogenic capacity was evaluated through colony formation assays. Flow cytometry was used to analyze cell cycle progression and apoptosis. Caspase-3/7 activity assays and annexin V/7-AAD staining confirmed the induction of apoptosis and pyroptosis. In vivo efficacy was assessed using a SAS xenograft model, and immunohistochemical analysis of xenograft tissue was performed to examine pyroptosis-related markers.
Results:
Okanin exhibited potent cytotoxic effects with IC50 values of 12.0 ± 0.8, 58.9 ± 18.7, 18.1 ± 5.3, and 43.2 ± 6.2 μM in SAS, SCC25, HSC3, and OEC-M1 cells, respectively. It caused dose- and time-dependent reductions in cell viability and significantly impaired clonogenic capacity. Flow cytometry revealed G2/M cell cycle arrest and increased sub-G1 population, indicating cell cycle disruption and death. Okanin induced both apoptosis and pyroptosis, as confirmed by caspase-3/7 activity and annexin V/7-AAD staining. In vivo, okanin reduced tumor growth and involved pyroptosis-related markers such as CASP1, GSDMC, GSDMD, and GSDME.
Conclusions:
Okanin demonstrates significant anticancer potential, particularly in oral cancer, by inducing both apoptosis and pyroptosis. Its efficacy in reducing tumor growth in vivo further supports its potential as a novel therapeutic option. Further mechanistic studies are needed to elucidate the pathways involved in okanin-mediated cell death and to explore its clinical applications.
Insights
Okanin, a flavonoid from Bidens pilosa, shows potent anticancer effects against oral cancer cells by inducing apoptosis and pyroptosis. In vivo studies confirmed its ability to reduce tumor growth, highlighting its therapeutic potential.
Area of Science:
- Natural Product Chemistry
- Oncology
- Molecular Biology
Background:
- Okanin, a flavonoid from Bidens pilosa L., possesses anti-inflammatory properties.
- Its anticancer potential in oral cancer is largely unexplored.
- Bidens pilosa is common in healthcare products and functional foods.
Purpose of the Study:
- Investigate okanin's effects on oral cancer cell lines.
- Evaluate okanin as a potential therapeutic agent for oral cancer.
Main Methods:
- Assessed cytotoxic effects (IC50) and clonogenic capacity of okanin on oral cancer cell lines (SAS, SCC25, HSC3, OEC-M1).
- Utilized flow cytometry to analyze cell cycle and apoptosis.
- Confirmed apoptosis and pyroptosis induction via caspase-3/7 activity and annexin V/7-AAD staining.
- Evaluated in vivo efficacy using a SAS xenograft model and analyzed pyroptosis markers via immunohistochemistry.
Main Results:
- Okanin demonstrated potent cytotoxicity against oral cancer cell lines.
- It inhibited cell viability, reduced clonogenic capacity, and induced G2/M cell cycle arrest.
- Okanin effectively induced both apoptosis and pyroptosis.
- In vivo, okanin suppressed tumor growth and modulated pyroptosis-related markers.
Conclusions:
- Okanin exhibits significant anticancer potential in oral cancer by inducing apoptosis and pyroptosis.
- Its demonstrated in vivo efficacy supports its potential as a novel therapeutic option.
- Further research is warranted to elucidate mechanisms and explore clinical applications.
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