Fig. 8

Schematic of the findings of the present study. CAFs-derived COMP induces EMT and stem cell-like phenotypes in HCC cells. However, RvD1, an endogenous proresolving and anti-inflammatory lipid mediator, binds to its receptor-FPR2 on the surface of CAFs, represses ROS mediated FOXM1 binding to the COMP promoter, and then inhibits COMP secretion to block this process