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CLG promotes mTOR/ULK1 pathway-mediated autophagy to inhibit OS development by inhibiting TRAF6-mediated FLT3

Xiongjie Huang1, Yanran Huang2, Bin Peng2

  • 1Affiliated Nanhua Hospital, South China University, Hengyang, Hunan Province, China.

Cancer Science
|August 9, 2024
PubMed

Insights

Corilagin (CLG) shows promise in treating osteosarcoma (OS). This study found CLG inhibits OS cell growth and tumor progression by promoting autophagy and apoptosis, offering a potential new therapy for this bone cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Corilagin (CLG) exhibits antitumor properties against various human cancers.
  • Osteosarcoma (OS) is a primary bone malignancy with limited effective therapeutic options.

Purpose of the Study:

  • To investigate the anti-osteosarcoma effects of Corilagin (CLG).
  • To elucidate the underlying molecular mechanisms of CLG action in OS cells and in vivo.

Main Methods:

  • Cell viability and proliferation assays (MTT, colony formation).
  • Cell cycle and apoptosis analysis via flow cytometry.
  • Co-immunoprecipitation to assess protein interactions (TRAF6-FLT3).
  • In vivo studies using mouse models of OS.

Main Results:

  • CLG significantly inhibited OS cell viability and proliferation in a dose-dependent manner.
  • CLG treatment promoted OS cell autophagy and apoptosis.
  • CLG was found to inhibit TRAF6-mediated FLT3 ubiquitination and degradation.
  • Overexpression of TRAF6 counteracted the anti-OS effects of CLG.
  • CLG administration suppressed OS tumor growth in mice by inducing autophagy-dependent apoptosis.

Conclusions:

  • CLG effectively inhibits osteosarcoma progression by promoting autophagy and apoptosis.
  • The mechanism involves the inhibition of TRAF6-mediated FLT3 ubiquitination, impacting the mTOR/ULK1 pathway.
  • CLG represents a potential therapeutic agent for osteosarcoma treatment.
Keywords:
FLT3TRAF6autophagycorilaginosteosarcoma

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