Fig 7.

Schematic model of the potential mechanisms involved in CRPC progression through the N-cadherin/c-Jun/NDRG1 axis. c-Jun is promoted by N-cadherin to induce heterodimerization with c-Fos to form AP-1. AP-1 forms a complex with AR and binds to TRE rather than ARE on the promoter of NDRG1. Then, AP-1 interacts with DNMT1 and further promotes DNA methylation to suppress the transcription of NDRG1. Furthermore, the decrease in NDRG1 expression reduces its role as an EMT marker and promotes the expression of N-cadherin to form a vicious cycle, ultimately leading to CRPC progression.