Polo-like kinase and survivin are esophageal tumor-specific promoters

被引:24
作者
Sato, F [1 ]
Abraham, JM
Yin, J
Kan, T
Ito, T
Mori, Y
Hamilton, JP
Jin, Z
Cheng, YL
Paun, B
Berki, AT
Wang, S
Shimada, Y
Meltzer, SJ
机构
[1] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA
[2] Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA
[3] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA
[4] Kyoto Univ, Grad Sch Med, Dept Surg & Surg Basic Sci, Kyoto 6068507, Japan
[5] Baltimore VA Med Ctr, Baltimore, MD 21201 USA
关键词
esophageal cancer; gene therapy; tumor-specific promoter; microarray;
D O I
10.1016/j.bbrc.2006.01.177
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
For developing successful cancer gene therapy strategies, tumor-specific gene delivery is essential. In this study, we used esophageal cancer (EC) cells to identify and evaluate esophageal tumor-specific gene promoters. Four genes (polo-like kinase-1/PLK, survivin/BIRC5, karyopherin alpha 2/KPNA2, and pituitary tumor transforming gene protein 1/PTTG1) were identified by a microarray analysis as highly expressed in EC cell lines vs. five normal organ tissues (liver, lung, kidney, brain, and heart). By quantitative RT-PCR, the average mRNA expression levels of these four genes in 20 primary ECs were 2.7-fold (PLK), 6.1-fold (survivin), 2.6-fold (KPNA2), and 2.4-fold (PTTG1) higher than that of each gene in 24 different normal organs. By dual luciferase assay, the promoter activity of PLK and survivin in EC cell lines was 18.9-fold and 28.5-fold higher, respectively, than in normal lung and renal cells. The promoters of PLK and survivin could be useful tools for developing EC-specific gene therapy vectors. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:465 / 471
页数:7
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