Story M T
Department of Urology, Medical College of Wisconsin, Milwaukee 53226, USA.
World J Urol. 1995;13(5):297-305. doi: 10.1007/BF00185973.
Growth of the prostate is controlled by androgen. However, there is information indicating that androgen may not act directly, but may act indirectly through polypeptide growth factors, to control prostate growth. This review will focus on the involvement of members of the fibroblast growth factor (FGF) family in this process. The properties of FGFs and FGF-receptors are described that implicate these molecules in growth control. Information is provided that prostate stromal cells synthesize FGF2 and FGF7. FGF2 is a potent mitogen for stromal cells; whereas, FGF7 is exclusively a mitogen for epithelial cells. Transforming growth factor beta (TGF beta), also produced by prostate cells, inhibit cell growth. This suggests that prostate growth is controlled by autocrine and paracrine mechanisms. Evidence is presented that altered FGF expression accompanies benign prostatic hyperplasia and prostate cancer. A model is proposed whereby androgen regulates TGF beta, influencing FGF2 and FGF7 expression, and in turn regulating growth of the prostatic stroma and epithelium. An imbalance in the influence of these growth factors may contribute to prostate disease.
前列腺的生长受雄激素控制。然而,有信息表明雄激素可能并非直接起作用,而是可能通过多肽生长因子间接发挥作用,从而控制前列腺的生长。本综述将聚焦于成纤维细胞生长因子(FGF)家族成员在这一过程中的参与情况。文中描述了FGF及其受体的特性,这些特性表明这些分子与生长控制有关。有信息表明前列腺基质细胞可合成FGF2和FGF7。FGF2是基质细胞的强效促有丝分裂原;而FGF7仅是上皮细胞的促有丝分裂原。前列腺细胞产生的转化生长因子β(TGFβ)可抑制细胞生长。这表明前列腺的生长受自分泌和旁分泌机制控制。有证据表明,FGF表达的改变与良性前列腺增生和前列腺癌相伴。提出了一个模型,即雄激素调节TGFβ,影响FGF2和FGF7的表达,进而调节前列腺基质和上皮的生长。这些生长因子影响的失衡可能导致前列腺疾病。