Many studies have shown that the overexpression of COX-2 leads to elevated endogenous PGE2, promoting breast cancer progression through multiple mechanisms: inactivation of host anti-tumor immune cells [102,103,104,105], enhanced cancer cell migration [70,106], invasiveness [70,107], tumor-associated angiogenesis [70,108], via multiple angiogenic pathways, and tumor-associated lymphangiogenesis [51,72,77,109] through the upregulation of VEGF-C and VEGF-D. This evidence concerns the gene VEGFC and neoplasm.