Janet Pittsenbarger

Conflicts of Interest The authors declare no conflicts of interest. Data Availability Statement The authors declare that all data supporting the findings of this study is available within the article and Supplemental Table 1 and from the corresponding author upon reasonable request. The prostate cancer TCGA data set [31], referenced in the study, is available in a public repository from the cBioPortal website (http://www.cbioportal.org/).

Conflicts of Interest The authors declare no conflicts of interest. Supporting Information Filename Description pros24895-sup-0001-Supplemental_Table_1.xlsx89.3 KB Supporting Table 1: Signature genes in clusters 0 – 3 based on scRNA-Seq of LNCaP cells without enzalutamide treatment. The signature gene is determined based on the CTL_avg_log2FC > 0.25. CTL = control condition without enzalutamide. Pct. 1 = percentage of expression in the corresponding cluster.

Abstract Most metastatic prostate cancers (PCa) initially depend on androgen for survival and proliferation. Thus, antiandrogen or castration therapies are the mainstay treatment. Although effective at first, androgen dependent PCa (ADPC) universally develops therapy resistance, thereby evolving to the incurable disease, called castration resistant PCa (CRPC). Currently, mechanisms underlying the emergence of CRPC from ADPC are largely unclear.