metastatic prostate cancer, castration-resistance, androgen receptor, signal pathway, non-coding rnas, immunomodulation, epigenetic modification, Medicine

By the time prostate cancer is diagnosed, most cases have metastasized. Androgen-deprivation therapy is an effective means of treating metastatic hormone-sensitive prostate cancer (mHSPC), but most patients eventually develop to metastatic castration-resistant prostate cancer (mCRPC). The mechanisms regulating the progression of mCRPC are still unclear, and androgen receptor (AR) signaling has been shown to play an important role in mCRPC through AR gene mutations, overexpression, co-regulatory factors, AR splice variants, and androgen resynthesis. A growing number of non-AR pathways have also been shown to affect the progression of mCRPC, including the Wnt and Hedgehog pathways. In addition, non-coding RNAs, immune related mechanisms and epigenetic modifications also play important roles in the pathogenesis of mCRPC. This article reviewed the relevant transition mechanism of mHSCP to mCRPC, in order to provide reference for related research.