COX-2 is overexpressed in most forms of epithelial cancer [56,57,58] leading to high levels of PGE2 production in the tumor microenvironment that facilitate tumor progression and metastasis by multiple mechanisms such as increased tumor cell migration, invasion, tumor-associated angiogenesis, and lymphangiogenesis and the induction of cancer stem cells (CSCs), mostly following the activation of EP2/EP4 receptors [53]. This evidence concerns the gene PTGS2 and neoplasm.