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VDUP1 potentiates Ras-mediated angiogenesis via ROS production in endothelial cells

Z H Piao1, S R Yoon, M S Kim

  • 1Korea Research Institute of Bioscience and Biotechnology, Stem Cell Research Center, Daejon, Republic of Korea.

Cellular and Molecular Biology (Noisy-Le-Grand, France)
|March 10, 2009
PubMed

Insights

Vitamin D3 up-regulated protein 1 (VDUP1) acts as a tumor suppressor by increasing reactive oxygen species (ROS) and promoting angiogenesis. Its role in Ras-mediated endothelial cell proliferation and tumor growth is significant.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Vitamin D3 up-regulated protein 1 (VDUP1) is a known tumor suppressor.
  • VDUP1 expression is frequently reduced in various cancer cells.
  • VDUP1 inhibits thioredoxin activity, leading to increased cellular reactive oxygen species (ROS).

Purpose of the Study:

  • To investigate the role of VDUP1 in angiogenesis and endothelial cell proliferation.
  • To understand the mechanism by which VDUP1 influences Ras-mediated processes.

Main Methods:

  • Overexpression of VDUP1 and the oncogene Ras in endothelial cells.
  • Measurement of ROS production.
  • Assessment of cell proliferation, resistance to anchorage-dependent cell death, and tube formation.
  • Use of ROS scavengers to evaluate the role of ROS.

Main Results:

  • Ras overexpression upregulates VDUP1 expression.
  • Enforced VDUP1 expression in Ras-overexpressing endothelial cells increases ROS production and proliferation.
  • VDUP1 overexpression enhances resistance to cell death and promotes tube formation in these cells.
  • ROS scavenging attenuates the effect of VDUP1 on tube formation.

Conclusions:

  • VDUP1 plays a role in Ras-mediated angiogenesis through ROS generation in endothelial cells.
  • VDUP1 may be a therapeutic target for cancers driven by Ras signaling.

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