PRL Signal Transduction in the Epithelial Compartment of Rat Prostate Maintained as Long-Term Organ Cultures in Vitro

摘要: Using long-term organ cultures of rat prostate tissue explants, we previously demonstrated that PRL both stimulates proliferation and acts as an androgen-independent suppressor apoptosis in epithelial cells, leading to hyperplasia. In this work delineate intracellular signaling molecules activated by identify candidate proteins are responsible for maintaining survival epithelium androgendeprived growth environment. We now show signal transducer activator transcription-5a (Stat5a) Stat5b become tyrosine phosphorylated response stimulation using culture experimental model. Stat5 was translocated the nuclei cells immunohistochemistry. Furthermore, EMSA showed PRLinducible binding Stat5a homodimers Stat5a/5b heterodimers element -casein gene promoter. Signaling Stat3, Stat1, MAPK, or protein kinase B, which can be other target were not tissue. continuously vivo, although they expressed varying degree separate lobes prostate. Collectively, our results suggest is primarily transduced via Stat5b. The pathway represents one mechanism, used possibly factors cytokines, supports viability during androgen deprivation. (Endocrinology 143: 228 –238, 2002)