雄激素受体(androgen receptor,AR)作为核内转录因子是前列腺癌中最常见的治疗靶标,在去势抵抗性前列腺癌(castration resistant prostate cancer,CRPC)中雄激素受体也起到了非常重要的作用。去势抵抗性前列腺癌的发生发展机制是当前的研究热点。表观遗传学的改变在前列腺癌的发展中具有重要作用。甲基化、乙酰化及非编码RNA可以通过对雄激素受体信号通路的调控促进或者抑制前列腺癌的发生发展。本文将近期关于前列腺癌雄激素受体信号通路表观遗传学的调节机制进行综述。
The androgen receptor (AR), a nuclear hormone and transcription factor, is the most therapeutic relevant target in pros-tate cancer (PCa) and in the castration-resistant prostate cancer (CRPC). Significant efforts have been focused on understanding the mechanisms involved in the development and progression of CRPC. Recent work has revealed the importance of epigenetic events in-cluding the regulation of AR signaling by methylation, acetylation, and non-coding RNA in the tumorigenesis and development of PCa. We summarize recent findings on the mechanisms of epigenetic regulation of AR signaling in PCa.