Basic fibroblast growth factor (bFGF) and transforming growth factor beta 1 (TGFP1) 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, 19931 that TGFPl 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 TGFPl upregulates the level of bFGF mRNA. A solution hybridization assay was used to quantitate bFGF mRNA. Treatment of PS for 6 hr with TGFPl (1 ng/ml) maximally stimulated bFGF mRNA expression. TGFP2 and TGFp3 were similarly active in upregulating bFGF mRNA. TGFPl 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 TGFpl-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 TGFPl 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 TGFP. It remains to be determined if an imbalance in this system in favor of stroma hyperplasia plays a role in the development of BPH.