Cyclin D1-AR Crosstalk: Potential Implications for Therapeutic Response in Prostate Cancer.

摘要

Prostate cancer is dependent on androgens and the androgen receptor (AR) for disease initiation, maintenance, and progression. Through work by our group and others, it has been shown that there is significant crosstalk between AR and the cell cycle machinery. Most importantly for our study, AR has been shown to induce the G1 to S phase transition in part via regulation of cyclin D1. Cyclin D1 serves as a rheostat to temper the pro-proliferative signaling of AR by directly binding to the receptor and inhibiting it s activity, thus inducing cell cycle arrest. As such, the AR-cyclin D1 crosstalk axis may serve to control the proliferative capacity of prostate cancer cells, and potentially alter the therapeutic efficacy of anti-cancer drugs. The data presented herein will demonstrate that cyclin D1 status does not impinge on the biological outcome in vitro of taxane-based therapy.