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Arsenic trioxide inhibits angiogenesis in vitro and in vivo by upregulating FoxO3a

Zhuo Sun1, Mingyan Li1, Lu Bai1

  • 1Department of Pathology, Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, No. 209 Tongshan Road, Xuzhou, Jiangsu, 221004, China.

Toxicology Letters
|August 18, 2019
PubMed

Insights

Arsenic trioxide (As2O3) inhibits tumor growth by blocking angiogenesis. This effect is mediated by the upregulation of FoxO3a, a key factor in controlling blood vessel formation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Arsenic trioxide (As2O3) is clinically used for leukemia and some solid tumors.
  • Its anti-tumor mechanisms, particularly anti-angiogenesis, are not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which As2O3 suppresses angiogenesis and tumor growth.
  • To investigate the role of FoxO3a in As2O3-mediated anti-angiogenesis.

Main Methods:

  • In vitro studies using human umbilical vein endothelial cells (HUVECs).
  • In vivo studies involving vascular endothelial cell-specific knockout of FoxO3a in mice.
  • Assessment of angiogenic potential and tumor growth.

Main Results:

  • As2O3 significantly inhibited HUVEC angiogenesis in vitro.
  • This inhibition was mediated by the upregulation of FoxO3a.
  • Knockdown of FoxO3a restored HUVEC angiogenic ability.
  • Vascular endothelial cell-specific knockout of FoxO3a in mice abrogated As2O3's anti-angiogenesis effect and led to tumor resistance.

Conclusions:

  • As2O3 suppresses angiogenesis and tumor growth through the upregulation of FoxO3a.
  • FoxO3a is a critical mediator of As2O3's anti-angiogenic and anti-tumor effects.
  • This study reveals a novel mechanism for As2O3 in cancer therapy.
Keywords:
AngiogenesisArsenic trioxideFoxO3a

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