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FIG. 7. mRNA and protein expression of the EP1, EP2, <t>EP3,</t> and EP4 receptors. mRNA expression of the EP1, EP2, EP3, and EP4 receptors in the human cholangiocarcinoma cell lines CCLP1 (A), HuCCT1 (B), and SG231 (C) was determined by reverse transcription-PCR. The protein levels of EP receptor subtypes in these cells were determined by Western blotting (D).
Ep3 Receptor Agonist Onoae, supplied by Ono Pharma, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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FIG. 7. mRNA and protein expression of the EP1, EP2, EP3, and EP4 receptors. mRNA expression of the EP1, EP2, EP3, and EP4 receptors in the human cholangiocarcinoma cell lines CCLP1 (A), HuCCT1 (B), and SG231 (C) was determined by reverse transcription-PCR. The protein levels of EP receptor subtypes in these cells were determined by Western blotting (D).

Journal: Journal of Biological Chemistry

Article Title: Cyclooxygenase-2-derived Prostaglandin E2 Promotes Human Cholangiocarcinoma Cell Growth and Invasion through EP1 Receptor-mediated Activation of the Epidermal Growth Factor Receptor and Akt

doi: 10.1074/jbc.m500562200

Figure Lengend Snippet: FIG. 7. mRNA and protein expression of the EP1, EP2, EP3, and EP4 receptors. mRNA expression of the EP1, EP2, EP3, and EP4 receptors in the human cholangiocarcinoma cell lines CCLP1 (A), HuCCT1 (B), and SG231 (C) was determined by reverse transcription-PCR. The protein levels of EP receptor subtypes in these cells were determined by Western blotting (D).

Article Snippet: The EP1 receptor agonist ONO-DI-004, the EP1 receptor antagonist ONO-8711, and the EP3 receptor agonist ONOAE-248 were provided by the Ono Pharmaceutical Co., Ltd. (Osaka, Japan).

Techniques: Expressing, Reverse Transcription, Western Blot

FIG. 8. Effect of activation or antisense inhibition of the EP1, EP2, EP3, and EP4 receptors on cholangiocarcinoma cell inva- sion. A, effect of EP receptor subtype agonists. CCLP1 cells (4 104) were seeded in the upper chamber, and medium containing vehicle, PGE2, or EP1 receptor agonist ONO-PI-004, the EP2 receptor agonist butaprost, the EP3 receptor agonist ONO-AE-248, or the EP4 receptor agonist PGE1 alcohol was added to the lower chamber. After 24 h, the cells on the upper surface of the filter were removed, and the filter was fixed and stained. The cells on the lower surface were counted under a microscope (magnification 50). Five fields were counted per filter, and 4 wells were used for each treatment. The experiment was repeated three times. Whereas PGE2 or ONO-DI-004 enhanced tumor cell inva- sion (*, p 0.01 compared with the control), agonists for the EP2, EP3, and EP4 receptors exhibited no effect. B, effect of antisense inhibition of EP receptor subtypes on PGE2-induced cholangiocarcinoma cell inva- sion. CCLP1 cells (4 104) transfected with antisense (As) oligonucleo- tides for the EP1, EP2, EP3, and EP4 receptors were seeded in the upper chamber; medium containing PGE2 or vehicle was added to the lower chamber. After 24 h, the cells on the upper surface of the filter were removed, and the filter was fixed and stained. The cells on the lower surface were counted under a microscope. Five fields were counted per filter, and 4 wells were used for each treatment. The data represent the average results from three experiments. PGE2-induced CCLP1 cell invasion was blocked by antisense inhibition of the EP1 receptor, but not by antisense inhibition of the EP2, EP3, or EP4 receptor. *, p 0.01 compared with the control; **, p 0.05 compared with PGE2 treatment of cells transfected with the control oligonucleotide. C, Western blots showing successful depletion of the EP1, EP3, and EP4 receptors in CCLP1 cells transfected with the corresponding antisense oligonucleo- tides. Western blotting for the EP2 receptor was not performed in EP2 receptor antisense cells because of the low basal expression of the EP2 receptor in CCLP1 cells.

Journal: Journal of Biological Chemistry

Article Title: Cyclooxygenase-2-derived Prostaglandin E2 Promotes Human Cholangiocarcinoma Cell Growth and Invasion through EP1 Receptor-mediated Activation of the Epidermal Growth Factor Receptor and Akt

doi: 10.1074/jbc.m500562200

Figure Lengend Snippet: FIG. 8. Effect of activation or antisense inhibition of the EP1, EP2, EP3, and EP4 receptors on cholangiocarcinoma cell inva- sion. A, effect of EP receptor subtype agonists. CCLP1 cells (4 104) were seeded in the upper chamber, and medium containing vehicle, PGE2, or EP1 receptor agonist ONO-PI-004, the EP2 receptor agonist butaprost, the EP3 receptor agonist ONO-AE-248, or the EP4 receptor agonist PGE1 alcohol was added to the lower chamber. After 24 h, the cells on the upper surface of the filter were removed, and the filter was fixed and stained. The cells on the lower surface were counted under a microscope (magnification 50). Five fields were counted per filter, and 4 wells were used for each treatment. The experiment was repeated three times. Whereas PGE2 or ONO-DI-004 enhanced tumor cell inva- sion (*, p 0.01 compared with the control), agonists for the EP2, EP3, and EP4 receptors exhibited no effect. B, effect of antisense inhibition of EP receptor subtypes on PGE2-induced cholangiocarcinoma cell inva- sion. CCLP1 cells (4 104) transfected with antisense (As) oligonucleo- tides for the EP1, EP2, EP3, and EP4 receptors were seeded in the upper chamber; medium containing PGE2 or vehicle was added to the lower chamber. After 24 h, the cells on the upper surface of the filter were removed, and the filter was fixed and stained. The cells on the lower surface were counted under a microscope. Five fields were counted per filter, and 4 wells were used for each treatment. The data represent the average results from three experiments. PGE2-induced CCLP1 cell invasion was blocked by antisense inhibition of the EP1 receptor, but not by antisense inhibition of the EP2, EP3, or EP4 receptor. *, p 0.01 compared with the control; **, p 0.05 compared with PGE2 treatment of cells transfected with the control oligonucleotide. C, Western blots showing successful depletion of the EP1, EP3, and EP4 receptors in CCLP1 cells transfected with the corresponding antisense oligonucleo- tides. Western blotting for the EP2 receptor was not performed in EP2 receptor antisense cells because of the low basal expression of the EP2 receptor in CCLP1 cells.

Article Snippet: The EP1 receptor agonist ONO-DI-004, the EP1 receptor antagonist ONO-8711, and the EP3 receptor agonist ONOAE-248 were provided by the Ono Pharmaceutical Co., Ltd. (Osaka, Japan).

Techniques: Activation Assay, Inhibition, Staining, Microscopy, Control, Transfection, Western Blot, Expressing

FIG. 10. Proposed mechanisms for COX-2- and PGE2-mediated cholangiocarcinoma cell invasion and proliferation. Prosta- glandin synthesis is controlled by coupled activation of cytosolic phos- pholipase A2 (cPLA2) and COX-2 along the cell membrane. The produced prostaglandins are released to the extracellular space by the prostaglandin transporter. The major prostaglandin in biliary epithe- lial and cancer cells is PGE2. After PGE2 is released into the extracel- lular space, it binds to the membrane G-protein-coupled EP receptors on the same cell (autocrine) or on a neighboring cell (paracrine). Al- though there are four types of PGE2 receptors (EP1, EP2, EP3, and EP4), our data show that the EP1 receptor plays a key role in COX-2- and PGE2-mediated cholangiocarcinoma cell invasion and proliferation and that this effect is mediated, at least in part, by activation of EGFR/Akt. On the other hand, activation of EGFR further enhances COX-2 expres- sion and PGE2 production, which further amplify COX-2/EP1/EGFR/ Akt signaling. The PGE2/EP1 receptor-induced transactivation of EGFR in cholangiocarcinoma cells is mediated, at least in part, through the c-Src-mediated intracellular mechanism; it remains unknown whether this process also involves extracellular release of endogenous EGFR ligand. AA, arachidonic acid.

Journal: Journal of Biological Chemistry

Article Title: Cyclooxygenase-2-derived Prostaglandin E2 Promotes Human Cholangiocarcinoma Cell Growth and Invasion through EP1 Receptor-mediated Activation of the Epidermal Growth Factor Receptor and Akt

doi: 10.1074/jbc.m500562200

Figure Lengend Snippet: FIG. 10. Proposed mechanisms for COX-2- and PGE2-mediated cholangiocarcinoma cell invasion and proliferation. Prosta- glandin synthesis is controlled by coupled activation of cytosolic phos- pholipase A2 (cPLA2) and COX-2 along the cell membrane. The produced prostaglandins are released to the extracellular space by the prostaglandin transporter. The major prostaglandin in biliary epithe- lial and cancer cells is PGE2. After PGE2 is released into the extracel- lular space, it binds to the membrane G-protein-coupled EP receptors on the same cell (autocrine) or on a neighboring cell (paracrine). Al- though there are four types of PGE2 receptors (EP1, EP2, EP3, and EP4), our data show that the EP1 receptor plays a key role in COX-2- and PGE2-mediated cholangiocarcinoma cell invasion and proliferation and that this effect is mediated, at least in part, by activation of EGFR/Akt. On the other hand, activation of EGFR further enhances COX-2 expres- sion and PGE2 production, which further amplify COX-2/EP1/EGFR/ Akt signaling. The PGE2/EP1 receptor-induced transactivation of EGFR in cholangiocarcinoma cells is mediated, at least in part, through the c-Src-mediated intracellular mechanism; it remains unknown whether this process also involves extracellular release of endogenous EGFR ligand. AA, arachidonic acid.

Article Snippet: The EP1 receptor agonist ONO-DI-004, the EP1 receptor antagonist ONO-8711, and the EP3 receptor agonist ONOAE-248 were provided by the Ono Pharmaceutical Co., Ltd. (Osaka, Japan).

Techniques: Activation Assay, Membrane, Produced