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Diosmetin inhibits cell proliferation and promotes apoptosis through STAT3/c-Myc signaling pathway in human

Rende Ning1, Guang Chen2, Run Fang2

  • 1Department of Orthopaedics, The Third Affiliated Hospital of Anhui Medical University, 390 Huaihe Road, Hefei, 230031, China. nrd192@qq.com.

Biological Research
|December 19, 2021
PubMed
Abstract

Insights

Diosmetin, a citrus bioflavonoid, effectively inhibits osteosarcoma cell growth and promotes apoptosis. It achieves this by suppressing the STAT3/c-Myc signaling pathway, offering potential as a new cancer therapy.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Diosmetin is a naturally occurring bioflavonoid found in citrus fruits.
  • Its potential antitumor effects, particularly in osteosarcoma, were previously unexplored.

Purpose of the Study:

  • To investigate the antitumor properties of diosmetin in human osteosarcoma cells.
  • To elucidate the underlying molecular mechanisms, including its effect on cell proliferation, apoptosis, and the STAT3/c-Myc pathway.

Main Methods:

  • Cell proliferation and apoptosis assays (colony formation, cell cycle, apoptosis analysis).
  • Western blot and immunoprecipitation to analyze protein expression and pathway activation.
  • Experiments conducted on Saos-2 and U2SO human osteosarcoma cell lines.

Main Results:

  • Diosmetin significantly inhibited osteosarcoma cell proliferation and induced apoptosis.
  • It caused cell cycle arrest at the G2/M phase.
  • Diosmetin downregulated anti-apoptotic proteins (Bcl-xL) and upregulated pro-apoptotic proteins (cleaved Caspase-3, cleaved-PARP, Bax).
  • It inhibited STAT3 phosphorylation, reduced c-Myc expression, and disrupted STAT3 molecular interactions.

Conclusions:

  • Diosmetin exhibits significant anti-osteosarcoma effects.
  • These effects are mediated by the suppression of cell proliferation and induction of apoptosis.
  • Inhibition of the STAT3/c-Myc signaling pathway is a key mechanism.
  • Diosmetin shows promise as a potential chemotherapeutic agent for osteosarcoma.
Keywords:
ApoptosisCell proliferationDiosmetinOsteosarcomaSignal transducer and activator of transcription 3 (STAT3)

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