We demonstrated that COX-2 over-expression leads to high endogenous PGE2 levels that promote breast cancer progression by multiple mechanisms: inactivation of host anti-tumor immune cells [30,31], enhanced cancer cell migration [47,48], invasiveness [47,49], tumor-associated angiogenesis [47] due to upregulation of angiogenic factors, and tumor-associated lymphangiogenesis [50,51,52,53] due to the upregulation of lymphangiogenic factors VEGF-C and -D. Here, VEGFC is linked to breast cancer.