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Chronic inflammation has a crucial role in cancer development and the progression of various tumors, including pancreatic ductal adenocarcinoma ( PDAC ). The arachidonate cascade is a major inflammatory pathway that produces several metabolites, such as prostaglandin E2. The enzyme 15‐hydroxyprostaglandin dehydrogenase (15‐ PGDH ) degrades prostaglandin and is frequently decreased in several types of cancer; however, the molecular mechanisms of 15‐ PGDH  suppression are unclear. The current study was carried out to elucidate the molecular mechanisms and clinical significance of 15‐ PGDH  suppression in  PDAC . Here, we showed that interleukin‐1β ( IL ‐1β), a pro‐inflammatory cytokine, downregulates 15‐ PGDH  expression in  PDAC  cells, and that  IL ‐1β expression was inversely correlated with 15‐ PGDH  levels in frozen  PDAC  tissues. We also found that activated macrophages produced  IL ‐1β and reduced 15‐ PGDH  expression in  PDAC  cells. Furthermore, the number of  CD 163‐positive tumor‐associated macrophages was shown to be inversely correlated with 15‐ PGDH  levels in  PDAC  cells by immunohistochemical staining of 107  PDAC  samples. Finally, we found that low 15‐ PGDH  expression was significantly associated with advanced tumors, presence of lymph node metastasis and nerve invasion, and poor prognosis in  PDAC  patients. Our results indicate that  IL ‐1β derived from  TAM s suppresses 15‐ PGDH  expression in  PDAC  cells, resulting in poor prognosis of  PDAC  patients.

Downregulation of 15‐hydroxyprostaglandin dehydrogenase by interleukin‐1β from activated macrophages leads to poor prognosis in pancreatic cancer