Therefore, given the role of the PDGF autocrine signaling in the maintenance of the FRA-1-driven EMT and cancer cell stemness [19], DDX5 might collaborate with FRA-1 by both direct mechanisms, mediated by the DDX5-FRA-1 interaction on chromatin [108], and indirect mechanisms, by sustaining the expression of PDGFR in TNBC cells [110]. Here, DDX5 is linked to cancer.