Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3101, USA.
Semin Immunopathol. 2013 Mar;35(2):123-37. doi: 10.1007/s00281-012-0342-8. Epub 2012 Sep 21.
Prostaglandin E(2) (PGE(2)) is a bioactive lipid that elicits a wide range of biological effects associated with inflammation and cancer. PGE(2) exerts diverse effects on cell proliferation, apoptosis, angiogenesis, inflammation, and immune surveillance. This review concentrates primarily on gastrointestinal cancers, where the actions of PGE(2) are most prominent, most likely due to the constant exposure to dietary and environmental insults and the intrinsic role of PGE(2) in tissue homeostasis. A discussion of recent efforts to elucidate the complex and interconnected pathways that link PGE(2) signaling with inflammation and cancer is provided, supported by the abundant literature showing a protective effect of NSAIDs and the therapeutic efficacy of targeting mPGES-1 or EP receptors for cancer prevention. However, suppressing PGE(2) formation as a means of providing chemoprotection against all cancers may not ultimately be tenable, undoubtedly the situation for patients with inflammatory bowel disease. Future studies to fully understand the complex role of PGE(2) in both inflammation and cancer will be required to develop novel strategies for cancer prevention that are both effective and safe.
前列腺素 E(2) (PGE(2)) 是一种生物活性脂质，可引发与炎症和癌症相关的广泛的生物学效应。PGE(2) 对细胞增殖、细胞凋亡、血管生成、炎症和免疫监视有不同的影响。本综述主要集中在胃肠道癌症上，因为 PGE(2) 的作用最为明显，这可能主要是由于持续暴露于饮食和环境刺激以及 PGE(2) 在组织平衡中的内在作用。本文讨论了最近为阐明 PGE(2) 信号与炎症和癌症之间复杂而相互关联的途径所做的努力，并提供了丰富的文献支持，这些文献表明 NSAIDs 具有保护作用，靶向 mPGES-1 或 EP 受体可预防癌症。然而，抑制 PGE(2) 的形成作为预防所有癌症的化学保护手段可能最终是不可行的，对于炎症性肠病患者来说情况无疑如此。为了开发有效且安全的癌症预防新策略，需要进一步研究以充分了解 PGE(2) 在炎症和癌症中的复杂作用。
