胰腺癌是一种高度恶性、预后极差的癌症。目前，已发现炎症因子前列腺素 E2（prostaglandin E2，PGE2）通过重塑肿瘤微环境，促进肿瘤的发生发展。一方面， PGE2可作用于胰腺癌微环境中的免疫细胞、肿瘤细胞、成纤维细胞及内皮细胞等，使之能更好地支持胰腺癌的生长、侵袭和远处转移。另一方面，肿瘤细胞释放的外泌体又影响了 PGE2的合成、释放和摄取，提高了 PGE2重塑微环境的能力。此外， PGE2还通过促进肿瘤再增殖和上皮间质转化等机制，增加了肿瘤细胞对治疗的抗性。因此， PGE2可能是干预胰腺癌的潜在治疗靶点。

Pancreatic cancer is a highly malignant disease with poor prognosis. Accumulating evidences indicate that prostaglandin E2 (PGE2) can promote cancer progressionreprogramming tumor microenvironment (TME). On one hand, PGE2 can regulate immune cells, tumor cells, cancer-associated fibroblasts and endothelial cells inTME to boost growth,invasion and metastasis of pancreatic cancer. On the otherhand,exosomes tumor cells influence the synthesis, release and uptake of PGE2 and enhance its reprogramming abilities. Furthermore, PGE2 even plays an important role in the development of therapy resistancestimulating tumor repopulation and inducing epithelial-mesenchymal transition. Hence, PGE2 might be a potential therapeutic target for intervention of pancreatic cancer.