Abstract
Cyclooxygenase-2 (COX-2), an inducible form of the enzyme that catalyzes the first step in the synthesis of prostanoids, is associated with inflammatory diseases and carcinogenesis, which is suspected to promote angiogenesis and tissue invasion of tumors and resistance to apoptosis. Meanwhile, COX-2 contributes to immune evasion and resistance to cancer immunotherapy, which plays a crucial role in the innate and adaptive immune response. The activity of COX-2-PGE2-EP signal pathway can suppress Dendritic cells (DCs), natural killer (NK), T cells, type-1 immunity excluding type-2 immunity which promote tumor immune evasion. COX-2 and the prostaglandin cascade play important roles in the “inflammogenesis of cancer”. In addition, COX-inhibitors can inhibit tumor immune evasion. Therefore, we can exert the COX-inhibitors to facilitate the patients to benefit from addition of COX-inhibitors to standard cytotoxic therapy.
Highlights
Human malignancies generally arise as the culmination of a multistep process that involves various somatic gene alterations
COX‐2: PGE2‐prostaglandin E receptors suppress innate and adaptive immunity COX-2: PGE2-prostaglandin E receptors contributes to immune evasion and resistance to cancer immunotherapy (Table 1), which have been reported to augment pro-tumorigenic type 2 lymphocyte [23]
It has been suggested that COX-inhibitors may sensitize type 1 immune responses via inhibiting M2 macrophage, T regulatory cells, MDSC; enhancing Dendritic cells (DCs), Natural Killer (NK), cytotoxic T-lymphocyte functions [42]
Summary
Human malignancies generally arise as the culmination of a multistep process that involves various somatic gene alterations. COX‐2: PGE2‐prostaglandin E receptors signal pathway Arachidonic acid (AA) is transformed into unstable intermediate PGG2, which is promptly converted into PGH2 by cyclooxygenases (COXs) and into five primary prostaglandins (PGD2, PGE2, PGF2α, PGI2, and TXA2) by cell-specific synthases. The actions of these prostanoid ligands are mediated by their engagement of specific cellsurface G-protein-coupled receptors designated EP1–4 for PGE2 [13]. COX‐2: PGE2‐prostaglandin E receptors suppress innate and adaptive immunity COX-2: PGE2-prostaglandin E receptors contributes to immune evasion and resistance to cancer immunotherapy (Table 1), which have been reported to augment pro-tumorigenic type 2 lymphocyte [23].
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