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• W2930716341 abstract "Abstract Elevated prostaglandin E 2 (PGE 2 ) levels are observed in colorectal cancer (CRC) patients, and this increase is associated with poor prognosis. Increased synthesis of PGE 2 in CRC has been shown to occur through COX-2-dependent mechanisms; however, loss of the PGE 2 -catabolizing enzyme, 15-hydroxyprostaglandin dehydrogenase (15-PGDH, HPGD ), in colonic tumors contributes to increased prostaglandin levels and poor patient survival. While loss of 15-PGDH can occur through transcriptional mechanisms, we demonstrate that 15-PGDH can be additionally regulated by a miRNA-mediated mechanism. We show that 15-PGDH and miR-21 are inversely correlated in CRC patients, with increased miR-21 levels associating with low 15-PGDH expression. 15-PGDH can be directly regulated by miR-21 through distinct sites in its 3′ untranslated region (3′UTR), and miR-21 expression in CRC cells attenuates 15-PGDH and promotes increased PGE 2 levels. Additionally, epithelial growth factor (EGF) signaling suppresses 15-PGDH expression while simultaneously enhancing miR-21 levels. miR-21 inhibition represses CRC cell proliferation, which is enhanced with EGF receptor (EGFR) inhibition. These findings present a novel regulatory mechanism of 15-PGDH by miR-21, and how dysregulated expression of miR-21 may contribute to loss of 15-PGDH expression and promote CRC progression via increased accumulation of PGE 2 ." @default.
• W2930716341 created "2019-04-11" @default.
• W2930716341 creator A5034221761 @default.
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• W2930716341 date "2019-04-01" @default.
• W2930716341 modified "2023-09-27" @default.
• W2930716341 title "miR-21-mediated regulation of 15-hydroxyprostaglandin dehydrogenase in colon cancer" @default.
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• W2930716341 doi "https://doi.org/10.1038/s41598-019-41862-2" @default.
• W2930716341 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6443653" @default.
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• W2930716341 hasPublicationYear "2019" @default.
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