RNA sequencing of 16D LTenza cells transduced with cMyc, shRb1, shTp53, shRb1_shTp53

The goal of this study was to determine how genetic alterations to AR inhibition-maintained prostate cancer cells alters transcriptional programs. We explored how MYC overexpression alters the transcriptional program of 16D cells maintained in enzalutamide for at least 2 months (LTenza) by transducing LTenza 16D cells with control (FUCRW) or MYC. To explore the effect of RB1 and TP53, we generated LTenza 16D cells with knockdown of RB1 and/or TP53 and compared these lines to control-transduced (shScr) LTenza 16D cells. Enzalutamide-naïve (DMSO-treated) cells were included to validate enzalutamide-induced inhibition of AR signaling in enzalutamide-maintained lines. Overall design: Comparative gene expression profiling analysis of RNA-seq data for untransduced DMSO-treated 16D cells and LTenza 16D cells transduced with shScr, FUCRW, MYC, shRB1, shTP53, or shRB1_shTP53