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Expression of basic fibroblast growth factor and its receptors FGFR1 and FGFR2 in human benign prostatic hyperplasia treated with finasteride
Author(s) -
Sáez Carmen,
GonzálezBaena Antonio C.,
Japón Miguel A.,
Giráldez Javier,
Segura Dolores I.,
RodríguezVallejo José M.,
GonzálezEsteban Jorge,
Miranda Gonzalo,
Torrubia Francisco
Publication year - 1999
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19990701)40:2<83::aid-pros3>3.0.co;2-n
Subject(s) - fibroblast growth factor receptor 1 , stromal cell , basic fibroblast growth factor , finasteride , immunohistochemistry , endocrinology , medicine , hyperplasia , prostate , fibroblast growth factor , basal (medicine) , androgen , biology , growth factor , receptor , hormone , cancer , insulin
BACKGROUND The development of benign prostatic hyperplasia (BPH) is an androgen‐dependent process which may be mediated by a number of locally produced growth factors. One of these, the basic fibroblast growth factor (bFGF or FGF2), has a mitogenic effect on prostatic stroma. High expression levels of bFGF have been reported in BPH. FGFR1 and FGFR2 receptors, that exhibit affinity for bFGF, have been identified in normal and hyperplastic prostate. Finasteride, a 5α‐reductase inhibitor, is an effective drug in the treatment of BPH, inducing regressive changes in the prostate of treated patients, even though its mechanisms of action are not yet completely elucidated. This study was designed to assess the effects of finasteride on the expression levels of bFGF, FGFR1, and FGFR2 in patients with BPH. METHODS The expression levels of bFGF, FGFR1, and FGFR2 in 9 patients with prostatic hyperplasia treated with finasteride were assessed by immunohistochemistry and reverse transcription‐polymerase chain reaction (RT‐PCR) analysis of mRNA expression and were compared with those of 9 control patients with untreated BPH. RESULTS Immunohistochemistry showed strong bFGF immunoreactivity in the prostatic stroma of untreated patients, this being somewhat weaker in the epithelium. In treated patients, epithelial immunoreactivity was practically negative, and a considerable reduction in stromal immunoreactivity was seen. These findings were also confirmed by RT‐PCR. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR2 exhibited strong stromal immunoreactivity, becoming weaker in the basal epithelium. No differences were seen in the expression of both receptors between the groups of treated and untreated patients. CONCLUSIONS A marked reduction in bFGF levels is seen in BPH treated with finasteride in comparison to untreated BPH. In our opinion, finasteride may act as a negative regulator of bFGF expression, counteracting the role of bFGF in the development of BPH. Prostate 40:83–88, 1999. © 1999 Wiley‐Liss, Inc.