Premium
Expression of p75 LNGFR and Trk neurotrophin receptors in normal and neoplastic human prostate
Author(s) -
Guate,
Marcel Fernández,
Lanzas,
Escaf,
J. Vega
Publication year - 1999
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1046/j.1464-410x.1999.00155.x
Subject(s) - tropomyosin receptor kinase a , trk receptor , neurotrophin , prostate , biology , stromal cell , low affinity nerve growth factor receptor , androgen receptor , nerve growth factor , tropomyosin receptor kinase b , tropomyosin receptor kinase c , prostate cancer , endocrinology , immunohistochemistry , medicine , cancer research , receptor , growth factor , neurotrophic factors , cancer , platelet derived growth factor receptor , immunology , biochemistry , genetics
Objective To analyse the occurrence and cell distribution of p75 LNGFR and Trk neurotrophin receptors in normal prostate, benign prostatic hypertrophy (BPH) and prostate carcinoma, and to determine the effect of androgen suppression on the expression of these proteins in prostate cancer samples. Materials and methods The study comprised formalin‐fixed and paraffin‐embedded material, obtained during surgery and from cadavers during removal of organs for transplantation. Light microscopy immunohistochemistry was carried out using polyclonal antibodies against Trks, and a monoclonal antibody against p75 LNGFR . General markers for epithelial and endocrine cells were assessed in parallel. Results TrkA immunoreactivity (IR) was restricted to the basal epithelial cells in some acini (37%). This pattern remained unchanged or IR extended to the whole acini in BPH, and varied widely in prostate cancer. In normal tissue and BPH, TrkC IR was detected exclusively in the stroma. Nevertheless, it progressively increased in the epithelial cells of well‐differentiated to moderately differentiated prostate carcinoma, whereas in stromal cells there were no substantial changes. TrkB IR was absent in all the samples. There was weak p75 LNGFR IR in normal epithelial cells, which increased in prostate cancer and to a lesser extent in BPH. Androgen suppression was ineffective in reversing TrkA modifications, whereas it caused a decrease in the expression of TrkC and p75 LNGFR . Conclusion The abnormal growth of prostatic epithelium is accompanied by increased TrkA expression and the induction of TrkC expression in epithelial cells. These results suggest that neurotrophins could be involved in the abnormal growth of the human prostate, acting through specific Trk signal‐transducing receptors whose expression is regulated by androgens.