al-8810 and Endometrial-Neoplasms

al-8810 has been researched along with Endometrial-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for al-8810 and Endometrial-Neoplasms

Article	Year
Prostaglandin E2 and F2alpha activate the FP receptor and up-regulate cyclooxygenase-2 expression via the cyclic AMP response element. Molecular and cellular endocrinology, 2008, Mar-26, Volume: 285, Issue:1-2 In endometrial adenocarcinomas COX-2 and F-series prostanoid (FP) receptor expression and prostanoid biosynthesis (PGE(2) and PGF(2alpha)) are elevated. In the present study, we investigated the effect of PGE(2) and PGF(2alpha) on the expression of COX-2 via the FP receptor in endometrial adenocarcinoma cells stably expressing the FP receptor (FPS cells). Using chemical inhibitors of intracellular signaling pathways, reporter gene assays and quantitative RT-PCR analysis, we show that PGE(2) and PGF(2alpha) can mobilize inositol 1,4,5-trisphosphate, induce ERK1/2 phosphorylation via the phospholipase Cbeta-protein kinase A-epidermal growth factor receptor pathway and induce cyclooxygenase-2 (COX-2) expression via the FP receptor. In addition we show that the PGE(2) or PGF(2alpha)-regulation of COX-2 via the FP receptor is mediated via the cAMP response element (CRE) binding site on the COX-2 promoter. These data indicate that PGE(2) and PGF(2alpha) biosynthesized locally within endometrial adenocarcinomas can regulate tumor cell function in an autocrine/paracrine manner via the FP receptor. Topics: Adenocarcinoma; Cell Line, Tumor; Cyclooxygenase 2; Dinoprost; Dinoprostone; Endometrial Neoplasms; Enzyme Activation; Enzyme Inhibitors; Extracellular Signal-Regulated MAP Kinases; Female; Gene Expression Regulation, Enzymologic; Genes, Reporter; Humans; Inositol 1,4,5-Trisphosphate; Promoter Regions, Genetic; Prostaglandin Antagonists; Receptors, Prostaglandin; Receptors, Prostaglandin E; Response Elements; Signal Transduction; Xanthones	2008

Article

Year

Prostaglandin E2 and F2alpha activate the FP receptor and up-regulate cyclooxygenase-2 expression via the cyclic AMP response element.

Molecular and cellular endocrinology, 2008, Mar-26, Volume: 285, Issue:1-2

In endometrial adenocarcinomas COX-2 and F-series prostanoid (FP) receptor expression and prostanoid biosynthesis (PGE(2) and PGF(2alpha)) are elevated. In the present study, we investigated the effect of PGE(2) and PGF(2alpha) on the expression of COX-2 via the FP receptor in endometrial adenocarcinoma cells stably expressing the FP receptor (FPS cells). Using chemical inhibitors of intracellular signaling pathways, reporter gene assays and quantitative RT-PCR analysis, we show that PGE(2) and PGF(2alpha) can mobilize inositol 1,4,5-trisphosphate, induce ERK1/2 phosphorylation via the phospholipase Cbeta-protein kinase A-epidermal growth factor receptor pathway and induce cyclooxygenase-2 (COX-2) expression via the FP receptor. In addition we show that the PGE(2) or PGF(2alpha)-regulation of COX-2 via the FP receptor is mediated via the cAMP response element (CRE) binding site on the COX-2 promoter. These data indicate that PGE(2) and PGF(2alpha) biosynthesized locally within endometrial adenocarcinomas can regulate tumor cell function in an autocrine/paracrine manner via the FP receptor.

Topics: Adenocarcinoma; Cell Line, Tumor; Cyclooxygenase 2; Dinoprost; Dinoprostone; Endometrial Neoplasms; Enzyme Activation; Enzyme Inhibitors; Extracellular Signal-Regulated MAP Kinases; Female; Gene Expression Regulation, Enzymologic; Genes, Reporter; Humans; Inositol 1,4,5-Trisphosphate; Promoter Regions, Genetic; Prostaglandin Antagonists; Receptors, Prostaglandin; Receptors, Prostaglandin E; Response Elements; Signal Transduction; Xanthones

2008