BioProject

Although AR-V7 has been intensively studied, it remains unclear whether AR-V7 and other AR splicing variants can specifically activate a distinctive transcriptional program from the full-length AR (AR-FL), and whether AR-V7 may play a role in accelerating the metastatic progression of castration-resistant PCa (CRPC). More...

Although AR-V7 has been intensively studied, it remains unclear whether AR-V7 and other AR splicing variants can specifically activate a distinctive transcriptional program from the full-length AR (AR-FL), and whether AR-V7 may play a role in accelerating the metastatic progression of castration-resistant PCa (CRPC). In this study, we hypothesize that AR-V7 can drive a distinct transcription program from AR-FL in CRPC condition. To test this, we used LNCaP model with inducible overexpression of AR-V7 or AR-V7-S81A to examine the transcriptional function of AR-V7 and the role of S81 phosphorylation on AR-V7 transcriptome. We also studied the endogenous AR-V7 transcriptome in CWR-22Rv1 cells using siRNA against AR-V7. Lastly, we used LNCaP model with inducible overexpression of AR-V567es to examine the AR-V567es transcriptome. Overall design: RNA-seq analyses were performed to examine genes reglated by AR-V7, AR-V7-S81A mutant, or ARv567es in LNCaP stable cell lines. The stable cells were generated by stably infecting LNCaP cells with tetracycline inducible overexpression of wild-type AR-V7 or S81A AR-V7 lentivirus and cumate inducible overexpression of AR-V567es lentivirus, and were grown in the medium containing 10% tetracycline-free FBS. Endogenous AR-V7 activity was examined by transient transfection of siNTC or siARV7 in CWR-22RV1. The experiments were performed under 5% homemone-depleted medium (CSS) and done in replicates. Less...