Androgen and its receptor (AR) are major drivers of prostate cancer (PCa), a leading cause of mortality in aging men. Thus, understanding the numerous mechanisms by which AR can promote the growth and proliferation of PCa cells and enable their escape from hormone-dependent therapies, eventually leading to metastasis and death of the patient, is essential to discover alternative therapeutic approaches. Recently, two structurally related members of the phosphatidylinositol 3-kinase-like protein kinase (PIKK) family, DNA-dependent protein kinase (DNA-PK) and mammalian target of rapamycin (mTOR), were shown to have a direct role in modulating AR activity on chromatin of PCa cells. In this review, the common features of DNA-PK and mTOR and the similarities in their noncanonical roles as transcription coregulators of the AR are highlighted. An outlook on how these findings could be translated into new approaches to manage and treat PCa is provided.

雄激素及其受体（AR）是前列腺癌（PCa）的主要驱动力，前列腺癌是衰老男性死亡的主要原因。因此，了解AR可以促进PCa细胞生长和增殖并使其脱离激素依赖性疗法从而最终导致患者转移和死亡的众多机制，对于发现其他治疗方法至关重要。最近，已显示磷脂酰肌醇3-激酶样蛋白激酶（PIKK）家族的两个结构相关成员，DNA依赖性蛋白激酶（DNA-PK）和雷帕霉素的哺乳动物靶标（mTOR）在调节AR中具有直接作用。对PCa细胞染色质的活性。在这篇综述中，着重介绍了DNA-PK和mTOR的共同特征，以及它们作为AR转录共调节子的非规范作用的相似性。