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Related Experiment Videos

Fisetin Promotes Autophagy in Osteosarcoma by Activating the ROS/FOXO3 Axis via Oxidative Stress.

Yujie Hu1, Lanyi Wei2, Jingjing Meng1

  • 1Department of Pharmacy, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Phytotherapy Research : PTR
|May 7, 2026
PubMed
Summary

Fisetin, a natural flavonoid, effectively inhibits osteosarcoma cell growth by targeting the ROS/FOXO3 pathway. This process induces autophagy and ferroptosis, offering a potential new therapy for this bone cancer.

Keywords:
FOXO3ROSautophagyfisetinorganoidsosteosarcoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Osteosarcoma presents treatment challenges due to metastasis and chemotherapy toxicity.
  • Fisetin, a dietary flavonoid, shows promise in various cancers, but its mechanism in osteosarcoma is unknown.

Purpose of the Study:

  • To investigate the anti-osteosarcoma effects of fisetin.
  • To elucidate the underlying molecular mechanisms of fisetin's action.

Main Methods:

  • Osteosarcoma cell and organoid proliferation assays.
  • RNA sequencing and immunofluorescence to identify key targets.
  • In vitro and in vivo experiments assessing proliferation, apoptosis, migration, autophagy, and ferroptosis.

Main Results:

  • Fisetin significantly inhibited osteosarcoma cell and organoid proliferation.
  • Fisetin targets the ROS/FOXO3 pathway, upregulating LC3 and inducing autophagy.
  • Autophagy activation by fisetin promoted ferroptosis, inhibiting tumor growth in vivo.

Conclusions:

  • Fisetin demonstrates potent anti-osteosarcoma activity.
  • The ROS/FOXO3-mediated autophagy and ferroptosis pathway is crucial for fisetin's efficacy.
  • Fisetin holds potential as a novel therapeutic agent for osteosarcoma.