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Regulation of basic fibroblast growth factor expression by transforming growth factor beta in cultured human prostate stromal cells
Author(s) -
Story Michael T.,
Hopp Kathleen A.,
Meier Daniel A.
Publication year - 1996
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(199604)28:4<219::aid-pros2>3.0.co;2-8
Subject(s) - basic fibroblast growth factor , stromal cell , autocrine signalling , transforming growth factor , endocrinology , biology , medicine , growth factor , transforming growth factor beta , hyperplasia , cancer research , chemistry , receptor
Basic fibroblast growth factor (bFGF) and transforming growth factor beta 1 (TGFβ1) are potential autocrine growth regulators of the prostatic stroma, and therefore may play a role in the development of benign prostatic hyperplasia (BPH). We reported [Story et al.: Prostate 22:183–197, 1993] that TGFβ1 increased bFGF and bFGF mRNA expression in cultured human prostate stromal cells (PS). The current study extends those studies and investigates the mechanism by which TGFβ1 upregulates the level of bFGF mRNA. A solution hybridization assay was used to quantitate bFGF mRNA. Treatment of PS for 6 hr with TGFβ1 (1 ng/ml) maximally stimulated bFGF mRNA expression. TGFβ2 and TGFβ3 were similarly active in upregulating bFGF mRNA. TGFβ1 or cycloheximide each increased bFGF mRNA about 3‐fold. The effect of these agents was not additive. This suggested that a labile protein was involved in processing bFGF mRNA. Determination of message stability indicated that the half‐life of bFGF mRNA in TGFβ1‐treated PS was 6.8 hr, as compared to 4.3 hr in untreated cells. The data indicated that posttranscriptional mechanisms, that increased message stability were, at least in part, responsible for upregulation of bFGF mRNA by TGFβ1 in PS. Our studies suggest that growth of the prostatic stroma is regulated by the interaction of members of two families of growth modulators, bFGF and TGFβ. It remains to be determined if an imbalance in this system in favor of stroma hyperplasia plays a role in the development of BPH. © 1996 Wiley‐Liss, Inc.