Abiraterone acetate (AA) is an inhibitor of androgen biosynthesis, though this cannot fully explain its efficacy against androgen-independent prostate cancer. Here, we demonstrate that androgen deprivation therapy depletes androgen-utilizing Corynebacterium spp. in prostate cancer patients and that oral AA further enriches for the health-associated commensal, Akkermansia muciniphila. Functional inferencing elucidates a coinciding increase in bacterial biosynthesis of vitamin K2 (an inhibitor of androgen dependent and independent tumor growth). These results are highly reproducible in a host-free gut model, excluding the possibility of immune involvement. Further investigation reveals that AA is metabolized by bacteria in vitro and that breakdown components selectively impact growth. We conclude that A. muciniphila is a key regulator of AA-mediated restructuring of microbial communities, and that this species may affect treatment response in castrate-resistant cohorts. Ongoing initiatives aimed at modulating the colonic microbiota of cancer patients may consider targeted delivery of poorly absorbed selective bacterial growth agents.

醋酸阿比特龙 (AA) 是雄激素生物合成的抑制剂，但这不能完全解释其对雄激素非依赖性前列腺癌的疗效。在这里，我们证明雄激素剥夺疗法会耗尽利用雄激素的棒状杆菌属。在前列腺癌患者中，口服 AA 进一步丰富了与健康相关的共生菌Akkermansia muciniphila. 功能推理阐明了维生素 K2（雄激素依赖性和非依赖性肿瘤生长抑制剂）的细菌生物合成同步增加。这些结果在无宿主肠道模型中具有高度可重复性，排除了免疫参与的可能性。进一步的研究表明，AA 在体外被细菌代谢，分解成分选择性地影响生长。我们的结论是A。muciniphila是 AA 介导的微生物群落重组的关键调节因子，并且该物种可能影响去势抵抗队列的治疗反应。旨在调节癌症患者结肠微生物群的持续举措可能会考虑靶向递送吸收不良的选择性细菌生长剂。