Impaired prostate tumorigenesis in Egr1-deficient mice

被引:151
作者
Abdulkadir, SA
Qu, ZC
Garabedian, E
Song, SK
Peters, TJ
Svaren, J
Carbone, JM
Naughton, CK
Catalona, WJ
Ackerman, JJH
Gordon, JI
Humphrey, PA
Milbrandt, J
机构
[1] Washington Univ, Dept Pathol, St Louis, MO 63119 USA
[2] Washington Univ, Dept Mol Biol, St Louis, MO 63119 USA
[3] Washington Univ, Dept Pharmacol, St Louis, MO 63119 USA
[4] Washington Univ, Dept Chem, St Louis, MO 63119 USA
[5] Univ Wisconsin, Dept Comparat Biosci, Madison, WI 53706 USA
[6] Washington Univ, Div Urol Surg, St Louis, MO 63119 USA
[7] Washington Univ, Dept Med, St Louis, MO 63119 USA
[8] Washington Univ, Dept Radiol, St Louis, MO 63119 USA
关键词
D O I
10.1038/83231
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
The transcription factor, early growth response protein 1 (ECR1), is overexpressed in a majority of human prostate cancers and is implicated in the regulation of several genes important for prostate tumor progression. Here we have assessed the effect of Egr1 deficiency on tumor development in two transgenic mouse models of prostate cancer (CR2-T-Ag and TRAMP). Using a combination of high-resolution magnetic resonance imaging and histopathological and survival analyses, we show that tumor progression was significantly impaired in Egr1(-/-) mice. Tumor initiation and tumor growth rate were not affected by the lack of Egr1; however, Egr1 deficiency significantly delayed the progression from prostatic intra-epithelial neoplasia to invasive carcinoma. These results indicate a unique role for Egr1 in regulating the transition from localized, carcinoma in situ to invasive carcinoma.
引用
收藏
页码:101 / 107
页数:7
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