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Metformin inhibits ovarian cancer via decreasing H3K27 trimethylation

Guiju Tang1, Jianfeng Guo1, Yapei Zhu1

  • 1Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.

International Journal of Oncology
|April 6, 2018
PubMed

Insights

Metformin, an AMPK activator, inhibits ovarian cancer cell proliferation and migration by reducing H3K27me3 epigenetic modifications. This study supports metformin use in non-diabetic ovarian cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Metformin is a widely used type II diabetes drug.
  • Its anticancer mechanisms, particularly in ovarian cancer, are under investigation.
  • Understanding these mechanisms can reveal new therapeutic strategies.

Purpose of the Study:

  • To investigate the effects of metformin on ovarian cancer cells in vitro.
  • To elucidate the molecular mechanisms underlying metformin's potential antitumor activity.
  • To explore the role of AMP-activated protein kinase (AMPK) and histone H3 lysine 27 trimethylation (H3K27me3) in metformin's action.

Main Methods:

  • Cell proliferation was assessed using the 5-ethynyl-20-deoxyuridine assay.
  • Apoptosis was detected by flow cytometry.
  • Cell migration capacity was evaluated using scratch wound healing and Transwell assays.
  • AMPK phosphorylation, H3K27me3, and polycomb repressor complex 2 (PRC2) levels were measured.
  • Experiments involved genetic manipulation (EZH2 overexpression) and pharmacological inhibition (Compound C).

Main Results:

  • Metformin inhibited ovarian cancer cell proliferation and migration while promoting apoptosis, especially under normoglycemic conditions.
  • Metformin treatment increased AMPK phosphorylation and reduced H3K27me3 and PRC2 levels.
  • Overexpression of EZH2 reversed metformin's effects, indicating H3K27me3's crucial role.
  • AMPK activation and H3K27me3 reduction by metformin were dependent on AMPK activity and glucose levels.
  • Similar effects were observed with another AMPK agonist, 2-deoxy-D-glucose.

Conclusions:

  • Metformin exerts antitumor effects in ovarian cancer by activating AMPK, which leads to the repression of H3K27me3 via targeting PRC2.
  • These findings highlight metformin's ability to alter epigenetic modifications.
  • Metformin shows promise for treating epithelial ovarian cancer patients without diabetes.

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