Androgen Deprivation Enhances PLZF-Repressed Cistrome that Promotes the Castration-Resistant Phenotype.

摘要

Androgen deprivation therapy (ADT) is an important therapeutic strategy which has a fundamental impact on prostate cancer biology. However, the mechanism by which ADT influences this negative androgenic regulation in CRPC development is unclear. Here, I identified an androgen-inducible tumor suppressor, Promyelocytic leukemia zinc finger protein (PLZF) which plays different roles in growth control, senescence, self-renewal, and tumor suppression in various cancer types. Interestingly, PLZF was reported as an androgen-responsive gene with anti-proliferative activity in prostate cancer cells. Moreover, decreased PLZF gene expression was observed in CRPC as compared to primary tumors, suggesting that loss of PLZF expression may have a role on CRPC development.