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MARCKSL1 exhibits anti-angiogenic effects through suppression of VEGFR-2-dependent Akt/PDK-1/mTOR phosphorylation

Boh-Ram Kim1, Seung-Hoon Lee2, Mi-Sun Park1

  • 1Research Institute, National Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do 410‑769, Republic of Korea.

Oncology Reports
|November 12, 2015
PubMed

Insights

Myristoylated alanine-rich C kinase substrate-like 1 (MARCKSL1) inhibits angiogenesis by blocking vascular endothelial growth factor receptor-2 (VEGFR-2) signaling. This novel anti-angiogenic agent suppresses tumor cell migration and proliferation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Myristoylated alanine-rich C kinase substrate-like 1 (MARCKSL1) is known for its role in apoptosis and antitumorigenic properties.
  • Angiogenesis, the formation of new blood vessels, is crucial for tumor growth and metastasis.

Purpose of the Study:

  • To investigate the anti-angiogenic effects of MARCKSL1.
  • To elucidate the molecular mechanisms by which MARCKSL1 inhibits angiogenesis-mediated cell migration and proliferation.

Main Methods:

  • Assessed MARCKSL1's impact on human umbilical vein endothelial cell (HUVEC) proliferation and capillary-like structure formation.
  • Analyzed MARCKSL1's effect on vascular endothelial growth factor receptor-2 (VEGFR-2) phosphorylation in ovarian tumorigenesis.
  • Measured MARCKSL1's influence on VEGF and hypoxia-inducible factor 1α (HIF-1α) expression.
  • Investigated MARCKSL1's role in the PI3K/Akt signaling pathway.

Main Results:

  • MARCKSL1 reduced VEGF-induced HUVEC proliferation and capillary-like structure formation.
  • MARCKSL1 disrupted VEGFR-2 phosphorylation and decreased VEGF and HIF-1α levels.
  • MARCKSL1 inhibited VEGF-induced phosphorylation of key PI3K/Akt pathway components (PDK-1, mTOR, TSC-2, p70S6K, GSK-3β).

Conclusions:

  • MARCKSL1 exhibits potent anti-angiogenic activity.
  • MARCKSL1 suppresses angiogenesis by inhibiting the Akt/PDK-1/mTOR pathway through interaction with VEGFR-2.

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