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Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2

Seung Bae Rho1, Yong Jung Song, Myong Cheol Lim

  • 1Research Institute, National Cancer Center, Ilsandong-gu, Goyang-si Gyeonggi-do, Republic of Korea. sbrho@ncc.re.kr

Cellular Signalling
|September 7, 2011
PubMed

Insights

Programmed cell death 6 (PDCD6) acts as an anti-angiogenic protein, inhibiting cell migration and proliferation. It targets the PI3K/mTOR pathway, suggesting a role in modulating cellular angiogenesis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Programmed cell death 6 (PDCD6) is known as a pro-apoptotic protein.
  • Its precise molecular functions, particularly in angiogenesis, remain incompletely understood.

Purpose of the Study:

  • To investigate the potential of PDCD6 as a novel anti-angiogenic protein.
  • To elucidate the molecular mechanisms underlying PDCD6's effects on angiogenesis-mediated cell growth.

Main Methods:

  • Utilized purified recombinant human PDCD6 in in vitro assays.
  • Assessed effects on cell migration, proliferation, invasion, and capillary-like tube formation.
  • Investigated downstream signaling pathways including PI3K/Akt/mTOR and VEGFR-2 interactions.

Main Results:

  • PDCD6 inhibited cell migration in a concentration- and time-dependent manner.
  • Overexpressed PDCD6 suppressed vascular endothelial growth factor (VEGF)-induced proliferation, invasion, and tube formation.
  • PDCD6 reduced phosphorylation of Akt, mTOR, GSK-3β, and p70S6K, and decreased cyclin D1 expression.
  • PDCD6 was found to bind to VEGFR-2, a key component of the PI3K/mTOR/P70S6K pathway.

Conclusions:

  • PDCD6 exhibits significant anti-angiogenic properties.
  • PDCD6 modulates cellular angiogenesis by inhibiting key signaling pathways, including PI3K/mTOR.
  • PDCD6 interacts with VEGFR-2, further supporting its role in regulating angiogenesis.

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