Prolonged exposure to (R)-bicalutamide generates a LNCaP subclone with alteration of mitochondrial genome.

Advanced prostate cancers, initially sensitive to androgen deprivation therapy, frequently progress to the castration-resistant prostate cancer phenotype (CRPC) through mechanisms not yet fully understood. In this study we investigated mitochondrial involvement in the establishment of refractoriness to hormone therapy in two human prostate cancer cell lines. Our data seem to indicate that the androgen-independent phenotype in our experimental model is due, at least in part, to alterations in mitochondrial dynamics and to a breakdown in the Drp-1-mediated mitochondrial network.