Fisetin induces apoptosis through mitochondrial apoptosis pathway in human uveal melanoma cells
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Updated: Feb 15, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Kai Wang1,2,3, Dan-Ning Hu4,5, Hui-Wen Lin6,7
1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Abstract:
Fisetin, a diatery flavonoid, been reported that possess anticancer effects in various cancers. The purpose of the study was to investigate the antitumor effects of fisetin in cultured uveal melanoma cell lines and compared with normal retinal pigment epithelial (RPE) cells. MTT assay was used for evaluating cytotoxic effects of fisetin. Flow cytometry study was used for the determination of apoptosis. JC-1 fluorescent reader was used to determine mitochondrial transmembrane potential changes. The results shown that fisetin dose-dependently decreased the cell viability of uveal melanoma cells but not influenced the cell viability of RPE cells. Apoptosis of uveal melanoma cells was induced by fisetin efficiently. Fisetin inhibited antiapoptotic Bcl-2 family proteins and damaged the mitochondrial transmembrane potential. The levels of proapoptotic Bcl-2 proteins, cytochrome c, and various caspase activities were increased by fisetin. In conclusion, fisetin induces apoptosis of uveal melanoma cells selectively and may be a promising agent to be explored for the treatment of uveal melanoma.
Insights
Fisetin, a dietary flavonoid, selectively induces apoptosis in uveal melanoma cells, sparing normal retinal pigment epithelial cells. This natural compound shows promise as a potential treatment for uveal melanoma.
Area of Science:
- Oncology
- Ophthalmology
- Pharmacology
Background:
- Fisetin is a dietary flavonoid with reported anticancer properties.
- Uveal melanoma is a primary intraocular malignancy with limited treatment options.
Purpose of the Study:
- To investigate the antitumor effects of fisetin on uveal melanoma cell lines.
- To compare the effects of fisetin on uveal melanoma cells versus normal retinal pigment epithelial (RPE) cells.
Main Methods:
- Cytotoxicity was assessed using MTT assays.
- Apoptosis was determined via flow cytometry.
- Mitochondrial transmembrane potential changes were measured using a JC-1 fluorescent reader.
Main Results:
- Fisetin dose-dependently reduced uveal melanoma cell viability without affecting RPE cells.
- Fisetin effectively induced apoptosis in uveal melanoma cells.
- Fisetin disrupted mitochondrial transmembrane potential and modulated Bcl-2 family proteins, increasing proapoptotic markers and caspase activity.
Conclusions:
- Fisetin selectively induces apoptosis in uveal melanoma cells.
- Fisetin demonstrates potential as a therapeutic agent for uveal melanoma treatment.
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