A novel treatment strategy for castration-refractory prostate cancer targeting cross-talk between NF-kB and an intranuclear steroid receptor superfamily

阐明一个全面的机制，通过该机制，大多数晚期前列腺癌患者对雄激素剥夺治疗有初步反应，但最终进展到去势抵抗状态，对于建立去势难治性前列腺癌（CRPC）的新治疗策略至关重要。我们从NF-κ B和核内类固醇受体超家族（包括雄激素受体、糖皮质激素受体和雌激素受体）之间的信号转导通路中的一些交叉对话的角度研究CRPC的机制。同时，我们针对串扰，采用多种方法抑制信号转导通路，建立了CRPC的综合治疗策略。因此，我们的研究表明，NF-κ B和核内类固醇受体超家族之间可能存在串扰，也表明抑制信号通路网络的串扰可能是治疗CRPC的新方法。

Elucidating a comprehensive mechanism through which most patients with advanced prostate cancer have an initial response to androgen deprivation therapy, but eventually progress to a castration-resistant state is critical to establish a novel treatment strategy for castration refractory prostate cancer (CRPC). We investigate the mechanism of CRPC from the perspective of some cross-talks in signal transduction pathway between NF-kB and an intranuclear steroid receptor superfamily containing androgen receptor, glucocorticoid receptor, and estrogen receptor. Also we target the cross-talk with various methods of inhibiting the signaling transduction pathway and established the integrated treatment strategy of CRPC. Consequently, our study made it clear that cross-talk between NF-kB and an intranuclear steroid receptor superfamily might existence, and also suggested inhibiting the cross-talk of signaling pathway network might be novel therapeutics for the management of CRPC.