Abstract 932: AR signaling differentially regulates the growth of prostate epithelial cells

Abstract

Abstract The prostate is an androgen-dependent organ. Androgen stimulates the growth of normal prostatic cells, as well as prostate cancer (PCa). However, AR signaling does not always promote cell proliferation, in some cases, it may even inhibit the growth of prostatic cells. In this study, we used NHPrE, a cell line derived from normal human prostate epithelia, to study how AR signaling modulates the growth of prostatic cells and to explore the mechanisms involved in AR's differential function in vitro and in vivo. Our results showed that inducing AR signaling in NHPrE cells suppressed their growth in vitro, concomitant with a reduction of Myc. In contrast, ectopic expression of AR in NHPrE cells induced the expression of Myc and pSTAT3 and drove the development of invasive PCa in vivo, suggesting a distinct in vivo function of AR signaling in prostatic cells. Furthermore, our data showed that the presence of prostate stromal cells over-rode androgen-mediated growth inhibition on NHPrE/AR cells in vitro; and IL-6/pSTAT3 was implicated in this stromal/epithelial communication. In conclusion, our study showed that AR signaling differentially regulated the growth of prostatic cells in vitro and in vivo through a mechanism that involved stromal/epithelial interactions. Citation Format: Xiuping Yu, Shu Yang. AR signaling differentially regulates the growth of prostate epithelial cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 932.