Abstract
The role of stromal‐epithelial (S‐E) interactions has been well characterized in the developing prostate, and is known to be dependent on the presence of a stromal androgen receptor (AR). We have utilized the LPB‐Tag mouse model of prostate tumor progression to study the role of S‐E interactions that occur in tumor development. We have crossed this transgene onto a vitamin D receptor (VDR) null background to elucidate cross‐talk between the VDR and AR and the role of testosterone in these interactions. Our data suggest that signaling through the VDR abrogates tumor progression in animals with low circulating testosterone; however this regulation is lost in androgen replete mice. To identify components of AR signaling that impinge on VDR‐mediated tumor cell growth, we isolated the stromal and epithelial compartments of the prostate by laser capture microdissection (LCM) in 15 week old mice with mid‐grade prostatic neoplasias. Total RNA was isolated from the LCM samples and subjected to microarray analysis. Bioinformatic analysis of the changes in stromal and epithelial gene expression and alterations in gene expression due to VDR ablation suggest that the VDR modulates the expression of several genes involved in cell cycle arrest (p21), cell proliferation (IGF, IGFR, PCNA), and apoptosis (survivin). This research is supported by R01 CA101114 to JW and MT.
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