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- W196466967 abstract "Aberrant expression of cyclooxygenase-2 (COX-2) has been observed in many human diseases including cancer and endometriosis. Overproduction of COX-2 derived eicosnoids, especially prostaglandin (PG) E2 not only enhances disease progression but also results in poor prognosis. However, mechanisms responsible for overexpression of COX-2 in these tissues are largely unknown. Herein, we provide evidence to demonstrate that aberrant expression of COX-2 in these tissues may be mediated by predisposition to hypoxia. Pre-exposure of cells to hypoxic stress result in increased sensitivity of COX-2 gene to IL-1β stimulation even after 48 h of reoxygenation. Promoter activity assay revealed that induction of COX-2 expression was mediated by upregulation of cox-2 gene by hypoxia-inducible factor-1α (HIF-1α). Similarly, treatment of cells with DFO, a chemical that will induce HIF-1α accumulation, also increased promoter sensitivity of cox-2 to IL-1β. The increase in cox-2 gene sensitivity by pre-exposure to hypoxia is also evident when other cox-2 stimulators such as EGF and PGE2 were used to treat the cells. Together, we have shown for the first time that overexpression of COX-2 in endometriotic stromal cells is likely due to hypoxia-mediated epigenomic modification of chromatin structure surrounding COX-2 promoter." @default.
- W196466967 created "2016-06-24" @default.
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- W196466967 date "2008-03-01" @default.
- W196466967 modified "2023-09-24" @default.
- W196466967 title "Hypoxia potentiates the accessibility of cyclooxygenase‐2 gene promoter to transcription factors" @default.
- W196466967 doi "https://doi.org/10.1096/fasebj.22.1_supplement.779.3" @default.
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