:
Prostate cancer (PCa) is the second most prevalent cancer and the fifth leading cause of cancer-related deaths
among men. Androgen deprivation therapy (ADT) is the most frequently used therapeutic strategy in PCa; however, the
development of resistance to ADT, known as castration-resistant prostate cancer (CRPC), continues to be a major obstacle
against successful treatment of PCa. The abnormal activation of the androgen receptor (AR) signaling pathway has been
found as one of the main contributing factors to the development of resistance in CRPC. Therefore, AR regulatory
strategies are urgently required to combat resistance. Recently, microRNAs (miRNAs) have been found as major AR
regulatory factors affecting ADT resistance. MiRNAs can target AR itself, AR-related genes, AR splice variants, ARrelated signaling pathways as well as cancer stem cells (CSCs), and play critical roles in regulating ADT resistance. Due
to their capability to affect various genes and signaling pathways, miRNAs are now being studied for their potential role
as a new therapeutic target in CRPC. It has been recommended that combination therapies including miRNAs and existing
drugs can synergistically decrease castration resistance. miRNAs have also prognostic values for ADT, and their
expression profiling in CRPC patients before therapeutic scheduling may enable the physician to diagnose patients who
are ADT-resistant. Overall, extant evidence obviously supports the predictive and therapeutic potential of miRNAs in
CRPC patients. This review summarizes the available information about the microRNA-mediated AR controlling
mechanisms involved in ADT resistance.