Androgen deprivation therapy (ADT) is a standard treatment for prostate cancer, delaying hormone-sensitive prostate cancer (HSPC). However, most patients eventually develop castration-resistant prostate cancer (CRPC), driven by androgen receptor (AR) signaling. In this study, we aim to investigate the potential role of HMGN1 in prostate cancer progression via AR interaction. Cancer cell lines were analyzed by RNAseq and mass spectrometry. Natively immunopreciptitated with HMGN1 eluents were separated in gradient gels and digested. Total of 735 proteins were identified from in-gel digested sample. In bioinformatic analysis, the CRPC proteins were relatively highly enriched in proteasome, fatty acid metabolism, and TCA cycle term. The upregulation of HMGN1 at the protein level, even in the absence of notable changes at the RNA level, suggests a potential role in enhancing AR signaling through the regulation of protein translation or stability. Further studies will investigate uncovering novel regulatory mechanisms and therapeutic targets.