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BioMed Research International
Volume 2013 (2013), Article ID 752603, 8 pages
Research Article

Soluble Flt-1 Gene Delivery in Acute Myeloid Leukemic Cells Mediating a Nonviral Gene Carrier

1Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia
2Department of Medical Microbiology, Faculty of Medicine, Ilam University of Medical Sciences, Ilam 69316, Iran
3UPM-MAKNA Cancer Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia
4Perdana University Graduate School of Medicine, Perdana University, 43400 Serdang, Selangor, Malaysia
5Department of Microbiology, College of Medicine, Al-Nahrain University, Baghdad, Iraq
6Hematology Department, School of Allied Health Medicine, Tehran University of Medical Sciences, Tehran, Iran

Received 25 May 2012; Revised 28 October 2012; Accepted 15 November 2012

Academic Editor: Richard Tucker

Copyright © 2013 Razieh Amini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in angiogenesis-mediated progression of acute myeloid leukemia (AML). Studies have reported the role of soluble form of fms-like tyrosine kinase (sFlT-1) delivery as an antitumor agent by inhibiting VEGF. This study investigates the outcome of delivery of a VEGF165 antagonist, soluble vascular endothelial growth factor receptor, namely sFLT-1, mediating lipofectamine 2000 in acute myeloid leukemic cells. A recombinant plasmid expressing sFLT-1 was constructed and transfected into the K562 and HL60 cells using lipofectamine 2000 transfection reagent. sFLT-1 expression/secretion in pVAX-sFLT-1 transfected cells was verified by RT-PCR and western blot. MTS assay was carried out to evaluate the effect of sFLT-1 on human umbilical vein endothelial cells and K562 and HL60 cells in vitro. Treatment with pVAX-sFLT-1 showed no association between sFLT-1 and proliferation of infected K562 and HL60 cells, while it demonstrated a significant inhibitory impact on the proliferation of HUVECs. The results of the current study imply that the combination of nonviral gene carrier and sFLT-1 possesses the potential to provide efficient tool for the antiangiogenic gene therapy of AML.