BRD4 Regulates Metastatic Potential of Castration-Resistant Prostate Cancer through AHNAK.

ABSTRACT: The inevitable progression of advanced prostate cancer to castration resistance, and ultimately to lethal metastatic disease, depends on primary or acquired resistance to conventional androgen deprivation therapy (ADT) and accumulated resistance strategies to evade androgen receptor (AR) suppression. In prostate cancer cells, AR adaptations that arise in response to ADT are not singular, but diverse, and include gene amplification, mutation, and even complete loss of receptor expression. Collectively, each of these AR adaptations contributes to a complex, heterogeneous, ADT-resistant tumor. Here, we examined prostate cancer cell lines that model common castration-resistant prostate cancer (CRPC) subtypes, each with different AR composition, and focused on novel regulators of tumor progress

SUBMITTER: Shafran JS 

PROVIDER: S-EPMC6677600 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature