PTGS2 and neoplasm: This dysregulated expression drives carcinogenesis through multiple mechanisms: excessive production of pro-inflammatory prostaglandin E2 (PGE2) promotes tumor cell proliferation, inhibits apoptosis, and facilitates angiogenesis; concurrently, COX-2-mediated remodeling of the TME induces immunosuppressive signaling, reduces anti-tumor immune surveillance, and enhances metastatic potential [353].