CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [ChIP-seq]

High-dose testosterone (high-T) treatment can effectively suppress the growth of castration-resistant prostate cancer (CRPC) in preclinical studies using patient-derived xenograft (PDX) models and in clinical trials of CRPC. However, the molecular basis for this treatment remains to be determined. In previous studies, we have shown that androgen receptor (AR) can function as a transcription repressor to suppress the expression of genes mediating DNA replication via recruitment of hypophosphorylated retinoblastoma protein (Rb). However, it is unclear how Rb globally mediates this transcriptional repressor activity of AR and contributes to the tumor-suppressive effect of high-dose androgen in CRPC. ChIP-seq of FOXA1, AR and P130 were performed in C42-tet-shRB cells with/out doxycycline. Samples of AR ChIP-seq were also treated with either ethanol (vehicle) or DHT (10nM) for 4 hours. ChIP-seq of RB and MYC were performed in C4-2 cells with/out DHT (10nM, 4hrs). All ChIP-seq samples contain replications.