Fisetin induces apoptosis through mitochondrial apoptosis pathway in human uveal melanoma cells

Kai Wang1,2,3, Dan-Ning Hu4,5, Hui-Wen Lin6,7

  • 1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.

Environmental Toxicology
|February 1, 2018
PubMed

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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