Stabilization of VEGF G-quadruplex and inhibition of angiogenesis by quindoline derivatives

Biochim Biophys Acta. 2014 Sep;1840(9):2970-7. doi: 10.1016/j.bbagen.2014.06.002. Epub 2014 Jun 12.

Abstract

Background: Angiogenesis is thought to be important in tumorigenesis and tumor progress. Vascular endothelial growth factor (VEGF) is a pluripotent cytokine and angiogenic growth factor that plays crucial roles in embryonic development and tumor progression. In many types of cancer, VEGF is overexpressed and is generally associated with tumor progression and survival rate. The polypurine/polypyrimidine sequence located upstream of the promoter region in the human VEGF gene can form specific parallel G-quadruplex structures, raising the possibility for transcriptional control of VEGF through G-quadruplex ligands.

Methods: PCR stop assay, circular dichroism (CD) spectra, RNA extraction and RT-PCR, enzyme-linked immunosorbent assay (ELISA), luciferase Assays, cell scrape test, xCELLigence real-time cell analysis (RTCA), and chick embryo chorioallantoic membrane (CAM) assay.

Results and conclusions: We found that quindoline derivatives can interact with the G-rich DNA sequences of the VEGF promoter to stabilize this G-quadruplex and suppress the transcription and expression of the VEGF protein. We also demonstrated that these derivatives exhibit potential anti-angiogenic activity in chick embryos and antitumor activity, including the inhibition of cell proliferation and migration.

General significance: Our new findings have significances not only for understanding the mechanism of the G-quadruplex ligands mediating the VEGF transcription inhibition, but also for exploring a new anti-tumor strategy to blocking the transcription of VEGF to inhibit the angiogenesis in cancer cells.

Keywords: Angiogenesis; Anti-tumor; G-quadruplex; Quindoline derivative; VEGF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaloids* / chemistry
  • Alkaloids* / pharmacokinetics
  • Alkaloids* / pharmacology
  • Animals
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cell Proliferation / drug effects
  • Chick Embryo
  • Circular Dichroism
  • CpG Islands*
  • Humans
  • Indoles* / chemistry
  • Indoles* / pharmacokinetics
  • Indoles* / pharmacology
  • Ligands
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / metabolism
  • Neovascularization, Pathologic / pathology
  • Promoter Regions, Genetic*
  • Quinolines* / chemistry
  • Quinolines* / pharmacokinetics
  • Quinolines* / pharmacology
  • Transcription, Genetic / drug effects*
  • Transcription, Genetic / genetics
  • Vascular Endothelial Growth Factor A / biosynthesis*
  • Vascular Endothelial Growth Factor A / genetics

Substances

  • Alkaloids
  • Indoles
  • Ligands
  • Quinolines
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • quindoline