Ptges, prostaglandin E synthase, is an enzyme involved in the arachidonic acid pathway, responsible for the synthesis of prostaglandin E2 (PGE2) [1,2,3,4,5,6,7,8,9]. PGE2 is a key mediator in various physiological and pathological processes, such as inflammation, cell growth, and immune response. Dysregulation of the Ptges-PGE2 axis has been linked to numerous diseases, highlighting its biological importance. Genetic models, especially knockout (KO) mouse models, can offer valuable insights into its functions.

In a Gprc5a-knockout mouse model, Ptges/PGE2 signaling was found to be highly associated with lung tumorigenesis and metastasis. Ptges-knockout in mouse lung tumor cells reduced their stemness and EMT-like features. Although they could still form tumors and lung metastasis in immune-deficient nude mice, they failed to do so in immune-competent mice, suggesting that the major role of Ptges/PGE2 signaling in tumorigenicity and lung metastasis is through immunosuppression [3]. In NSCLC, knockdown of Ptges in lung cancer cells suppressed cell migration, reduced the expression of CSC markers, tumor sphere formation, colony-forming activity, tumorigenicity, and lung metastasis in vivo [5].

In conclusion, Ptges plays a crucial role in the synthesis of PGE2, which is involved in various disease-related processes such as tumorigenesis, metastasis, and immunosuppression. Studies using Ptges KO mouse models have revealed its significance in these disease areas, providing important insights into the underlying mechanisms and potential therapeutic targets.