SRP493458 PRJNA1084009 GSE260921 Effect of NFIB knockdown on gene expression in the prostate cancer cells. The widespread use of androgen receptor (AR) signaling inhibitors has led to an increased incidence of AR-negative castration-resistant prostate cancer (CRPC), limiting effective treatment and patient survival. A more comprehensive understanding of the molecular mechanisms supporting AR-negative CRPC could reveal therapeutic vulnerabilities to improve treatment.In this study, we discovered that the transcription factor nuclear factor I/B (NFIB) was upregulated in AR-negative CRPC patient tumors and cell lines and was positively associated with an epithelial-to-mesenchymal transition (EMT) phenotype. Loss of NFIB inhibited EMT process and reduced migration of CRPC cells. Overall design: To investigate the regulatory mechanisms of NFIB promoting EMT process and metastasis of AR-negative prostate cancer, we constructed stable cell line with continuous suppression of NFIB in AR-negative DU145 cells using the lentivirus-shRNA. DU145-shNFIB and DU145-shNC cells with two respective replicates were then analyed on gene expression platform. GSE260921