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Updated: May 20, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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Triptonide inhibits the progression of oral squamous cell carcinoma by suppressing the TRIP13/c-Myc axis

Hongbo Zhang1, Zheng Wei2, Shengwei Han1

  • 1Department of Oral and Maxillofacial Surgery, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.

Neoplasma
|March 31, 2025
PubMed

Insights

Triptonide, derived from Tripterygium wilfordii Hook. F., inhibits oral squamous cell carcinoma (OSCC) progression by downregulating thyroid hormone receptor interactor 13 (TRIP13), which in turn suppresses c-Myc expression. This reveals a novel therapeutic pathway for OSCC treatment.

Area of Science:

  • Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Tripterygium wilfordii Hook. F. extract contains triptonide, known for anticancer properties.
  • The effect of triptonide on oral squamous cell carcinoma (OSCC) remains uninvestigated.
  • Understanding triptonide's mechanism in OSCC is crucial for potential therapeutic applications.

Purpose of the Study:

  • To investigate the inhibitory effect of triptonide on OSCC progression.
  • To elucidate the underlying molecular mechanism of triptonide's action in OSCC.
  • To identify potential therapeutic targets for OSCC treatment.

Main Methods:

  • Cell proliferation, migration, and invasion assays (CCK-8, EdU, wound healing, Transwell).
  • In vivo xenograft tumor models.
  • Molecular analyses including western blotting, qRT-PCR, immunohistochemistry, and RNA-seq.
  • Gene knockdown and overexpression studies using siRNA and plasmids.

Main Results:

  • Triptonide significantly inhibited OSCC cell progression in vitro and in vivo.
  • Triptonide suppressed the expression of c-Myc in OSCC cells.
  • RNA-seq identified thyroid hormone receptor interactor 13 (TRIP13) as a key differentially expressed gene.
  • TRIP13 knockdown reduced OSCC progression, while TRIP13 overexpression partially rescued triptonide-induced c-Myc downregulation.

Conclusions:

  • Triptonide inhibits OSCC progression by suppressing TRIP13 expression, leading to reduced c-Myc levels.
  • TRIP13 acts upstream of c-Myc in the triptonide-mediated signaling pathway.
  • Triptonide demonstrates potential as a therapeutic agent for oral squamous cell carcinoma.

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