CDK4/6 inhibition enhances the tumor-suppressive activity of high-dose androgens in castration-resistant prostate cancer [RNA-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. Overall design: All xenograft tumor samples for RNA-seq cells were isolated at the end of study. Note: two C4-2-tet-shRB xenograft experiments (with/out doxycycline) were done independently. All RNA-seq samples contain replications.