Moreover, the HIC1-deleted breast cancer cells can secret CXCL14 to its cognate receptor GPR85 on mammary fibroblasts in the microenvironment, and activate fibroblasts through the ERK1/2, Akt, and neddylation signaling pathways, whereas the activated fibroblasts can facilitate breast cancer progression through inducing epithelial-mesenchymal transition (EMT) by the CCL17/CCR4 axis (39). This evidence concerns the gene MAPK3 and breast cancer.