Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Mechanisms involved in PGE 2 -induced transactivation of the epidermal growth factor receptor in MH 1 C 1 hepatocarcinoma cells

doi: 10.1186/1756-9966-31-72

Figure Lengend Snippet: Effect of different prostaglandin receptor inhibitors in MH 1 C 1 cells. A ) The EP4 inhibitor L-161982 (10 μM) was added 30 min prior to stimulation with PGE 2 (100 μM) for 5 min. B ) The EP1 inhibitor SC51322 (5 or 10 μM) was added 30 minutes prior to stimulation with PGE 2 (100 μM) for 5 min. C ) The FP inhibitor AL8810 (10 or 100 μM) was added 30 minutes prior to stimulation with PGE 2 (100 μM) for 5 min. All blots are representative of three independent experiments. D ) Effect of AL8810 (100 μM) on accumulation of inositol phosphates after stimulation with increasing concentrations of fluprostenol for 30 minutes in the presence of 15 mM LiCl. The data shown are mean ± S.E.M of four independent experiments.

Article Snippet: AL8810 (9α,15R-dihydroxy-11β-fluoro-15-(2,3-dihydro-1 H-inden-2-yl)-16,17,18,19,20-pentanor-prosta-5Z,13E-dien-1-oic acid),L161982 (N-[[4'-[[3-butyl-1,5-dihydro-5-oxo-1-[2-(trifluoromethyl)phenyl]-4 H-1,2,4-triazol-4-yl]methyl][1,1'-biphenyl]-2-yl]sulfonyl]-3-methyl-2-thiophenecarboxamide), (+)fluprostenol, and prostaglandin E 2 (PGE 2 ) were from Cayman Chemical (Ann Arbor, MI).

Techniques:

Journal: Genes to Cells

Article Title: Prostaglandin E 2 and its receptor EP2 trigger signaling that contributes to YAP‐mediated cell competition

doi: 10.1111/gtc.12750

Figure Lengend Snippet: Effects of prostaglandin E 2 and various receptor agonists or antagonists on the apical extrusion of YAP (5SA) cells. (a–d) Quantification of percentages of apically extruded cells in cocultures of labeled YAP (5SA) cells that were mixed 1:50 with unlabeled normal MDCK cells and treated with Dox plus the indicated compounds for various times starting at 24 hr postseeding. Controls were cocultures incubated for the appropriate times with/without Dox in the absence of the indicated compounds. (a) Cells were treated for 24 hr with Dox plus ONO‐8711 (EP1 antagonist, 10 μM), PF‐04418948 (EP2 antagonist, 10 μM), L‐798106 (EP3 antagonist, 10 μM) or ONO‐AE3‐208 (EP4 antagonist, 10 μM). (b) Cells were treated for 16 hr with Dox plus butaprost (EP2 agonist, 10 μM). (c) Cells were treated for 24 hr with Dox and NS398 (50 μM) plus butaprost (10 μM), U‐46619 (TP agonist, 100 nM), Fluprostenol (FP agonist, 10 μM), sulprostone (EP1/3 agonist, 10 μM), BW‐245C (DP agonist, 10 μM) or Cicaprost (IP agonist, 10 μM). (d) Cells were treated for 24 hr with Dox and NS398 (50 μM) plus PGE 2 (1 µM or 5 µM). For (a)–(d), data are the mean + SD ( n = 3/group) of three independent experiments

Article Snippet: The chemical inhibitors PF‐4708671 (PZ0143, 10 μM), indomethacin (I7378, 10–20 μM), L‐798106 (L4545, 10 μM), forskolin (F3917, 10 μM) and N 6 ,2′‐O‐Dibutyryladenosine 3′,5′‐cyclic monophosphate sodium salt (db‐cAMP) (D0627, 1–3 mM) were all purchased from Sigma‐Aldrich; NS398 (ab120295, 10–50 μM) and H‐89 (ab143787, 10–50 μM) were from Abcam; PGE 2 (163‐10814, 1–5 μM) was from Wako; SC‐560 (70340, 10–50 μM), ONO‐8711 (14070, 10 μM), PF‐04418948 (15016, 10 μM), butaprost (13740, 10 μM), U‐46619 (16450, 100 nM), 15(s)‐Fluprostenol (16787, 10 μM), sulprostone (14765, 10 μM), BW245C (12050, 10 μM) and Cicaprost (16831, 10 μM) were all from Cayman Chemical Company; ONO‐AE3‐208 (CS‐0315, 10 μM) was from Chemscene; and LY294002 (10 μM) and rapamycin (0.1 μM) were from Calbiochem.

Techniques: Labeling, Incubation