15-Hydroxyprostaglandin dehydrogenase is down-regulated in colorectal cancer.

摘要: Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates biosynthesis breakdown, most reports examining have focused solely on the cyclooxygenase-dependent formation this bioactive lipid. Enzymatic degradation involves NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). The present study examined a range normal tissues in human mouse found high 15-PGDH large intestine. By contrast, expression is decreased colorectal carcinoma lines other malignancies such as breast lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh ApcMin+/– adenomas. activity correlates genetic disruption completely blocks production urinary metabolite. Finally, are significantly down-regulated carcinomas to matched tissue. In summary, results suggest novel suppressive role for due loss during progression.