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. 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.