Häggström S, Wikström P, Bergh A, Damber J E
Department of Urology and Andrology, Umeå University, Sweden.
Prostate. 1998 Jul 1;36(2):71-9. doi: 10.1002/(sici)1097-0045(19980701)36:2<71::aid-pros1>3.0.co;2-h.
Angiogenesis is important for prostate organogenesis and prostate cancer progression. It is not yet known whether androgens promote part of their control of prostate structure and function by influencing angiogenesis. The aim of this study was to explore the possible androgenic regulation of the angiogenic factor vascular endothelial growth factor (VEGF) and its receptors flt-1 and flk-1/KDR in the rat ventral prostate (VP) and Dunning R3327 PAP adenocarcinoma.
RNA was prepared from VP and tumors of intact and castrated rats. VEGF, flt-1, and flk-1/KDR mRNA levels were determined using competitive RT-PCR.
VEGF121, VEGF165, and VEGF189 together with flt-1 and flk-1/KDR mRNA were detected. The VEGF, but not flt-1 mRNA levels were significantly decreased in the VP after castration. The Dunning tumor expressed high levels of mRNA for VEGF and its receptors compared to the VP. The flt-1 mRNA level in the tumor increased after castration, while the VEGF mRNA levels were unchanged.
Decreased mRNA expression of VEGF, but not flt-1, was found in the rat VP after castration. However, in the Dunning tumor, castration did not alter the expression of VEGF mRNA. Moreover, elevated levels of both mRNA for VEGF and its receptors relative to the VP were observed, indicating that the VEGF system may be important for Dunning tumor development.
血管生成对于前列腺器官形成和前列腺癌进展至关重要。雄激素是否通过影响血管生成来部分控制前列腺的结构和功能尚不清楚。本研究的目的是探讨雄激素对大鼠腹侧前列腺（VP）和邓宁R3327 PAP腺癌中血管生成因子血管内皮生长因子（VEGF）及其受体flt-1和flk-1/KDR的可能调节作用。
从完整和去势大鼠的VP和肿瘤中提取RNA。使用竞争性逆转录聚合酶链反应（RT-PCR）测定VEGF、flt-1和flk-1/KDR mRNA水平。
检测到VEGF121、VEGF165和VEGF189以及flt-1和flk-1/KDR mRNA。去势后VP中VEGF mRNA水平显著降低，但flt-1 mRNA水平未降低。与VP相比，邓宁肿瘤中VEGF及其受体的mRNA表达水平较高。去势后肿瘤中flt-1 mRNA水平升高，而VEGF mRNA水平未改变。
去势后大鼠VP中VEGF mRNA表达降低，但flt-1 mRNA未降低。然而，在邓宁肿瘤中，去势并未改变VEGF mRNA的表达。此外，相对于VP，观察到VEGF及其受体的mRNA水平均升高，表明VEGF系统可能对邓宁肿瘤的发展很重要。
