Microarray analysis of differential gene expression in androgen independent prostate cancer using a metastatic human prostate cancer cell line model

被引:6
|
作者
Balaji, KC
Rao, PS
Smith, DJ
Louis, S
Smith, LM
Sherman, S
Bacich, D
O'Keefe, D
机构
[1] Univ Nebraska, Med Ctr, Div Urol, Dept Surg, Omaha, NE 68198 USA
[2] So Illinois Univ, Sch Med, Div Urol, Dept Surg, Springfield, IL 62702 USA
[3] Univ Nebraska, Sch Med, Dept Prevent & Societal Med, Omaha, NE 68198 USA
[4] Univ Nebraska, Sch Med, Eppley Res Inst, Dept Pathol & Microbiol, Omaha, NE 68198 USA
[5] Cleveland Clin Fdn, Dept Canc Biol, Cleveland, OH 44195 USA
关键词
differential gene expression; prostate cancer; androgen independence; microarray; cell line model;
D O I
10.1016/S1078-1439(03)00238-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Progression to androgen independence (AI) leading to uncontrolled cell growth is the main cause of death in prostate cancer. While almost all patients with metastatic prostate cancer will initially respond to anti-androgen treatments, the majority will fail hormonal treatments in less than 2 yrs. Both genetic and epigenetic alterations in gene expression contribute significantly to the development of AI. To investigate this we have used an in vitro cell line model of AI prostate cancer from which we have identified a number of differentially expressed genes associated with progression to AI in prostate cancer. We used an in vitro cell line model of AI prostate cancer, to study differential gene expression using cDNA microarray analysis and corroborated the microarray results with Ribonuclease Protection Assay (RPA). Approximately 4480 out of 7075 (63.3%) cDNA cloned genes were differentially expressed, of which, 6 genes were differentially expressed by at least fivefold. RPA was used to corroborate the microarray results for the five most highly differentially expressed genes. Using an in vitro cell line model and microarray analysis we have identified a number of candidate genes for further investigation in AI prostate cancer. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:313 / 320
页数:8
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