Fig. 7

KDM5 proteins drive breast cancer progression. EGLN2-catalyzed hydroxylation of H3P13 promotes the binding of KDM5A to H3K4me3 thereby inhibiting the expression of the Wnt signaling inhibitor DDK1 and indirectly promoting Wnt signaling-induced cell cycle. KDM5A also suppresses the expression of the tumor suppressor gene P16 thereby promoting the migration of breast cancer cells. KDM5B impairs the immune response by inhibiting STING and promoting cancer cell migration by inhibiting SOX17. KDM5B interacts with EMSY to inhibit miRNA-31 thereby promoting tumorigenesis. In addition, KDM5B enhances cancer cell EMT by promoting MALAT1. KDM5C inhibits the expression of immune genes to promote tumorigenesis, and it interacts with RACK7 to promote the expression of ER target genes, which promotes cancer cell proliferation. KDM5C inhibits the expression of BRMS1 in a demethylation-dependent manner to promote cell migration