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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, S48 (Printed in Great Britain)
Meeting Abstract
Liver-specific expression of an exogenous gene controlled by human apolipoprotein A-I promoter
Yurong Hu1, Xueling Ren1, Hui Wang1, Yue Ma1, Lei Wang1, Yingying Shen1, Kazuhiro Oka2, Zhenzhong Zhang1* and Yun Zhang1*
1School of Pharmacy, Zhengzhou University, 100 Science Road, Zhengzhou, PR China, and 2Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Huston, TX 77030, USA

Liver-specific gene therapy is advantageous to minimize the possible adverse effects caused by non-target gene expression. The CMV promoter of the enhanced green fluorescent protein (EGFP) expressing plasmid CMV-EGFP was replaced with the liver-specific promoter apolipoprotein A-I (ApoAI) generating ApoAI-EGFP plasmid. In vitro expression experiments performed in various cell lines including HepG2, SMMC-7721, MCF-7, ACC-2 and Lo2 indicated that pCMV-EGFP treatment caused gene expression in all the cell lines, whereas pApoAI-EGFP treatment only induced EGFP expression in cells of liver origin including the liver cancer cells HepG2 and SMMC-7721 and the normal liver cells Lo2. Either pCMV-EGFP or pApoAI-EGFP was formulated as pegylated immuno-lipopolyplexes (PILP), a novel and efficient gene delivery system. Following intravenous administration of the PILP in H22 tumor-bearing mice, there was significant EGFP expression in liver, tumor, spleen, brain and lung in the pCMV-EGFP treated mice, whereas in the pApoAI-EGFP treated mice there was only gene expression in liver and tumor and the non-liver organ gene expression was eliminated. This study suggests that the use of the PILP technology and liver-specific promoter enables efficient and liver-specific expression of an exogenous gene.

*correspondence author

Published online 1 August 2010, doi:10.1042/CBI034S048b

© The Author(s) Journal compilation © 2010 Portland Press Limited

ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)