Trichodermin inhibits the growth of oral cancer through apoptosis-induced mitochondrial dysfunction and

Hsien-Lin Chen1, Yi-Hao Lo2, Chieh-Liang Lin3

  • 1Division of General Surgery, Department of Surgery, Chi Mei Medical Center, Liouying, Tainan 73657, Taiwan.

Insights

Trichodermin (TCD) effectively inhibits oral squamous cell carcinoma (OSCC) growth by suppressing proliferation, migration, and inducing apoptosis. This study highlights TCD as a potential therapeutic agent for OSCC treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Trichodermin (TCD), a trichothecene, is known to inhibit eukaryotic protein synthesis.
  • The effects of TCD on oral squamous cell carcinoma (OSCC) and its mechanisms are not well understood.

Purpose of the Study:

  • To investigate the anti-cancer effects of TCD on human OSCC cells.
  • To elucidate the molecular mechanisms underlying TCD's action in OSCC.

Main Methods:

  • MTT and colony formation assays for proliferation.
  • Migration and invasion assays, Western blotting for protein analysis.
  • Flow cytometry for cell cycle analysis, apoptosis assays, and mitochondrial function assessment.
  • Zebrafish OSCC xenotransplantation model for in vivo efficacy.

Main Results:

  • TCD suppressed OSCC cell proliferation, migration, and invasion by downregulating matrix metalloproteinase 9.
  • TCD induced G2/M phase arrest and caspase-dependent apoptosis, while reducing x-linked inhibitor of apoptosis.
  • TCD impaired mitochondrial function and decreased levels of HDAC-2, p-STAT3, and p-NF-κB.
  • TCD significantly inhibited OSCC tumor growth in a zebrafish model.

Conclusions:

  • TCD exhibits significant anti-cancer properties against OSCC cells in vitro and in vivo.
  • TCD acts through multiple pathways, including apoptosis induction and metabolic dysfunction.
  • TCD represents a promising novel therapeutic strategy for oral squamous cell carcinoma treatment.

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