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Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing

Ying Gao1, Sarah L Miles2, Piyali Dasgupta2

  • 1Tea Research Institute, Chinese Academy of Agricultural Sciences, Hangzhou 310008, China.

International Journal of Molecular Sciences
|June 2, 2021
PubMed

Insights

Trichodermin effectively suppressed ovarian cancer cell proliferation and decelerated tumor growth in vivo. This trichothecene shows potential for treating ovarian cancer by inducing cell cycle arrest and targeting c-Myc.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Ovarian cancer is a leading cause of gynecological cancer deaths, often diagnosed late and developing chemoresistance.
  • Trichodermin, a trichothecene from *Trichoderma viride*, inhibits protein synthesis, but its effect on ovarian cancer was unknown.

Purpose of the Study:

  • To investigate the potential of trichodermin as a therapeutic agent against ovarian cancer.
  • To elucidate the molecular mechanisms underlying trichodermin's anti-ovarian cancer activity.

Main Methods:

  • Assessing trichodermin's effect on ovarian cancer cell lines (A2780/CP70, OVCAR-3) and normal cells (IOSE 346) proliferation.
  • Analyzing cell cycle distribution, apoptosis, and expression of key cell cycle regulatory proteins (cyclin D1, CDK4, CDK2, pRB, Cdc25A, c-Myc, p21, p27, p16).
  • Evaluating trichodermin's anti-tumor efficacy in a mouse xenograft model.

Main Results:

  • Trichodermin (≥0.5 µM) significantly inhibited ovarian cancer cell proliferation with minimal impact on normal cells.
  • Trichodermin induced G0/G1 cell cycle arrest, primarily by downregulating cyclin D1, CDK4, CDK2, pRB, Cdc25A, and c-Myc.
  • c-Myc was identified as a key target, mediating trichodermin's regulation of Cdc25A and downstream proteins; its overexpression reduced trichodermin's efficacy.
  • Trichodermin treatment decelerated tumor growth in vivo.

Conclusions:

  • Trichodermin demonstrates significant anti-ovarian cancer activity both in vitro and in vivo.
  • The compound's mechanism involves inducing cell cycle arrest via c-Myc and Cdc25A pathway modulation.
  • Trichodermin presents a promising candidate for novel ovarian cancer therapeutics.
Keywords:
A2780/CP70 cellsCdc25AOVCAR-3 cellsc-Myccell cycle arresttrichodermin

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