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Fucoidan Enhances Cisplatin-induced Effects on SCC-25 Human Oral Cancer Cells by Inhibiting the PI3K/AKT Pathway
Ching-Huey Yang1,2,3, Yun-Ching Chang4, Chung-Chi Hsu4
1Department of Traditional Chinese Medicine, Pingtung Veterans General Hospital, Pingtung, Taiwan, R.O.C.
Anticancer Research
|August 30, 2023
Summary
Fucoidan enhances cisplatin sensitivity in oral cancer cells by inhibiting AKT signaling, promoting apoptosis, and improving treatment outcomes. This combination therapy shows promise for clinical application in oral cancer treatment.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Cisplatin is a key drug for oral cancer treatment.
- Oral cancer cells can develop resistance to cisplatin, leading to poor patient prognosis.
- Fucoidan, derived from brown seaweed, exhibits anticancer properties against various cancer types.
Purpose of the Study:
- To investigate if fucoidan can increase oral cancer cell sensitivity to cisplatin.
- To explore the underlying molecular mechanisms of fucoidan's effect on cisplatin sensitivity.
Main Methods:
- SCC-25 oral cancer cells were treated with fucoidan, cisplatin, or a combination.
- Cell viability was assessed using MTT assays.
- Apoptosis and autophagy markers were analyzed via ELISA and immunoblotting.
Main Results:
- Combined fucoidan and cisplatin significantly reduced SCC-25 cell survival compared to cisplatin alone.
- Cotreatment increased apoptosis markers (caspase-8, -9, -3, cleaved PARP) but not autophagy markers (beclin, ATG12-ATG5).
- Fucoidan inhibited cisplatin-induced AKT activation, leading to increased apoptosis.
Conclusions:
- Fucoidan potentiates cisplatin's effects by inhibiting the PI3K/AKT pathway.
- This combination therapy may offer a new strategy to improve oral cancer treatment outcomes.
