Development of a miR-92a delivery system for anti-angiogenesis-based cancer therapy

J Gene Med. 2013 Jan;15(1):20-7. doi: 10.1002/jgm.2690.

Abstract

Background: RNA interference has received much attention as a novel therapeutic strategy. MicroRNA (miRNA) appears to be promising as a novel nucleic-acid medicine because it is able to suppress a series of protein expression that relates to a specific event such as angiogenesis. In the present study, we used dicetyl phosphate-tetraethylenepentamine-based polycation liposomes (TEPA-PCL) as a delivery system for miR-92a, one of the miRNAs regulating angiogenesis, and attempted to deliver miR-92a to angiogenic endothelial cells for the development of cancer therapy by anti-angiogenesis.

Methods: Cholesterol-grafted miR-92a (miR-92a-C) was bound to TEPA-PCL, and the ratio of nitrogen of TEPA-PCL to phosphorus of miR-92a-C (N/P ratio) was optimized. This complex was transfected into human umbilical vein endothelial cells (HUVECs), and the intracellular localization of miR-92a-C was observed under a confocal laser-scanning microscope by the use of fluorescein isothiocyanate-labeled miR-92a-C. After transfection of HUVECs with miR-92a-C/TEPA-PCL, the expression of miR-92a-target proteins (e.g. integrin α5, mitogen-activated protein kinase kinase 4, sphingosine-1-phosphate receptor 1) was examined by western blotting, and a tube formation assay was performed.

Results: The complex of miR-92a-C with TEPA-PCL was formed and miR-92a-C remained stable with TEPA-PCL at the N/P ratio of 10. After transfection of HUVECs with miR-92a-C complex, miR-92a-C spread into the whole cytoplasm of the cells without any change of cellular morphology, and the expression of several proteins encoded by miR-92a-target genes was suppressed. Furthermore, the capability of forming capillary tubes was impaired in complex-treated HUVECs.

Conclusions: We have developed a miR-92a delivery system into angiogenic endothelial cells by the use of TEPA-PCL. These results suggest that miR-92a-C/TEPA-PCL is promising for the treatment of tumors via the suppression of angiogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / metabolism*
  • Blotting, Western
  • Cells, Cultured
  • Ethylenediamines / pharmacology
  • Gene Expression Regulation
  • Gene Knockdown Techniques
  • Gene Transfer Techniques*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Integrin alpha5 / genetics
  • Integrin alpha5 / metabolism
  • Liposomes
  • MAP Kinase Kinase 4 / genetics
  • MAP Kinase Kinase 4 / metabolism
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Microscopy, Confocal
  • Neoplasms / therapy
  • Neovascularization, Pathologic / therapy
  • RNA Interference
  • Receptors, Lysosphingolipid / genetics
  • Receptors, Lysosphingolipid / metabolism
  • Sphingosine-1-Phosphate Receptors

Substances

  • Angiogenesis Inhibitors
  • Ethylenediamines
  • Integrin alpha5
  • Liposomes
  • MIRN92 microRNA, human
  • MicroRNAs
  • Receptors, Lysosphingolipid
  • S1PR1 protein, human
  • Sphingosine-1-Phosphate Receptors
  • MAP Kinase Kinase 4
  • tetraethylenepentamine