EXPRESSION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR AND ITS RECEPTORS INTHE RAT VENTRAL PROSTATE AND DUNNING R3327 PAP ADENOCARCINOMA BEFORE AND AFTER CASTRATION

Citation
S. Haggstrom et al., EXPRESSION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR AND ITS RECEPTORS INTHE RAT VENTRAL PROSTATE AND DUNNING R3327 PAP ADENOCARCINOMA BEFORE AND AFTER CASTRATION, The Prostate, 36(2), 1998, pp. 71-79
Citations number
57
Categorie Soggetti
Urology & Nephrology","Endocrynology & Metabolism
Journal title
ISSN journal
02704137
Volume
36
Issue
2
Year of publication
1998
Pages
71 - 79
Database
ISI
SICI code
0270-4137(1998)36:2<71:EOVEGA>2.0.ZU;2-4
Abstract
BACKGROUND. Angiogenesis is important for prostate organogenesis and p rostate cancer progression. It is not yet known whether androgens prom ote part of their control of prostate structure and function by influe ncing angiogenesis. The aim of this study was to explore the possible androgenic regulation of the angiogenic factor vascular endothelial gr owth factor (VEGF) and its receptors flt-1 and flk-1/KDR in the rat ve ntral prostate (VP) and Dunning R3327 PAP adenocarcinoma. METHODS. RNA was prepared from VP and tumors of intact and castrated rats. VEGF, f lt-1, and flk-1/KDR mRNA levels were determined using competitive RT-P CR. RESULTS. VEGF(121), VEGF(165), and VEGF(189) together with flt-1 a nd flk-1/KDR mRNA were detected. The VEGF, but not flt-1 mRNA levels w ere significantly decreased in the VP after castration. The Dunning tu mor expressed high levels of mRNA for VEGF and its receptors compared to the VP. The flt-1 mRNA level in the tumor increased after castratio n, while the VEGF mRNA levels were unchanged. CONCLUSIONS. Decreased m RNA expression of VEGF, but not flt-1, was found in the rat VP after c astration. However, in the Dunning tumor, castration did not alter the expression of VEGF mRNA. Moreover, elevated levels of both mRNA for V EGF and its receptors relative to the VP were observed, indicating tha t the VEGF system may be important for Dunning tumor development. (C) 1998 Wiley-Liss, Inc.