BioProject

Castration resistant prostate cancer (CRPC) develops resistance to antiandrogens affecting Androgen Receptor (AR) signaling through a variety of mechanism. More...

Castration resistant prostate cancer (CRPC) develops resistance to antiandrogens affecting Androgen Receptor (AR) signaling through a variety of mechanism. Because of this, the efficacy of androgen receptor targeted therapy remains limited for many patients with CRPC. We developed C42B-enzalutamide (ENZU) and resistance cells to study changes in transcriptomic profile compared to parental cells. Overall design: Genome wide expression of prostate cancer cells (C42B and C42B-enzalutamide resistant cells) were determined using RNA-seq. The RNA-seq experiment were performed with C42B cells were recurrently exposed to increasing concentrations of enzalutamide (1~ 20 μM) by passage in media containing enzalutamide for 6 months in 10% FBS and stored for further analysis. The resistant cells generated from 20 µM enzalutamide were always maintained in media containing 5µM enzalutamide were referred to as C42B Enzu (C42B enzalutamide resistance). Parental C42B cells treated with 1% DMSO were passaged alongside the enzalutamide treated cells as an appropriate control.C42B and C42B-Enzu cells were maintained in RPMI 1640 with 10% FBS. All cells were maintained at 37°C in a humidified incubator with 5% carbon dioxide. Less...