Luteolin inhibits angiogenesis by blocking Gas6/Axl signaling pathway

Int J Oncol. 2017 Aug;51(2):677-685. doi: 10.3892/ijo.2017.4041. Epub 2017 Jun 13.

Abstract

Growth arrest-specific protein 6 (Gas6) induces the activation of Axl receptor tyrosine kinase (Axl), which plays an important role in angiogenic processes, including proliferation, migration, invasion, tube formation and pericyte recruitment of endothelial cells. The inhibition of Gas6/Axl pathway has been demonstrated to be an effective anti-angiogenic therapy. Luteolin, which is a natural active flavonoid, has been reported to possess anti-angiogenic effects. However, the underlying mechanism of luteolin in anti-angiogenesis is not fully understood. Herein, we report that luteolin significantly inhibited the Gas6-induced proliferation, migration, invasion and tube formation of human microvascular endothelial cells (HMEC‑1s) in vitro, and suppressed the Gas6-induced recruitment of human brain vascular pericytes (HBVPs) to the endothelial tubes. Luteolin also suppressed Gas6-induced microvessel sprouting in aortic ring assay and neovascularization in chick chorioallantoic membrane assay. The anti-angiogenic effect of luteolin may be associated with the inhibition of the Gas6/Axl pathway and its downstream phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways. Taken together, the present study provides new evidence regarding an anti-angiogenic mechanism of luteolin, and supports the notion that the dietary intake of luteolin contributes to the treatment of pathological angiogenesis.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Axl Receptor Tyrosine Kinase
  • Cell Line
  • Cell Proliferation / drug effects
  • Chick Embryo
  • Chorioallantoic Membrane / drug effects
  • Chorioallantoic Membrane / growth & development
  • Endothelial Cells / drug effects
  • Endothelial Cells / pathology
  • Humans
  • Intercellular Signaling Peptides and Proteins / genetics*
  • Luteolin / administration & dosage*
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / pathology
  • Oncogene Protein v-akt / genetics
  • Pericytes / drug effects
  • Pericytes / pathology
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphorylation
  • Proto-Oncogene Proteins / genetics*
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / genetics

Substances

  • Intercellular Signaling Peptides and Proteins
  • Proto-Oncogene Proteins
  • growth arrest-specific protein 6
  • Receptor Protein-Tyrosine Kinases
  • Oncogene Protein v-akt
  • TOR Serine-Threonine Kinases
  • Luteolin
  • Axl Receptor Tyrosine Kinase
  • AXL protein, human