In this issue of Cancer Cell, Su et al. demonstrate that epigenetic reprogramming by Polycomb Repressive Complex 1 (PRC1) promotes an inflammatory tumor microenvironment in a subtype of metastatic prostate cancer, and show that a PRC1 inhibitor can synergize with immune checkpoint inhibitors to suppress metastasis in mouse models.
A catalytic inhibitor of PRC1 cooperates with immune checkpoint therapy to reverse these processes and suppress metastasis in genetically engineered mouse transplantation models of DNPC.
In addition, the PCa patients with PRC1 overexpression more frequently had high Gleason score, advanced pathological stage, positive metastasis, short overall survival time and positive PSA failure than those with low Gleason score, early pathological stage, negative metastasis, long overall survival time and negative PSA failure (all P<0.05).