• Corpus ID: 10808311

Eicosanoid synthesis by cultured human urothelial cells: potential role in bladder cancer.

  title={Eicosanoid synthesis by cultured human urothelial cells: potential role in bladder cancer.},
  author={A Prouvost Danon and Terry V. Zenser and Denise Thomasson and Bernard B. Davis},
  journal={Cancer research},
  volume={46 11},
Prostaglandin (PG) H synthase and eicosanoid products of arachidonic acid metabolism have been implicated in several steps in the carcinogenic process. This study assessed these parameters using primary cultures of human urothelial cells. To determine the possible presence of permeability barriers to agonist stimulation, incubations were performed with adherent cells in the presence or absence of thioglycolate pretreatment or with cell suspensions. No evidence for permeability barriers was… 

Figures and Tables from this paper

Mechanism of 12-O-tetradecanoylphorbol-13-acetate enhanced metabolism of arachidonic acid in dog urothelial cells.

The mechanism of 12-O-tetradecanoylphorbol-13-acetate enhanced arachidonic acid metabolism was investigated in dog urothelial cells and additive effects were observed with respect to release of [3H]arachidic acid, 3H-prostaglandins, and radioimmunoassayable PGE2, suggesting that separate pathways may be involved in enhanced arACHidonic Acid metabolism demonstrated with different agonists.

Mechanism of 12-0-Tetradecanoylphorbol-13-acetate Enhanced Metabolism of Arachidonic Acid in Dog Urothelial Cells1

Two path ways may be involved in enhanced arachidonic acid metabolism demon strated with different agonists, according to experiments investigated in dog urothelial cells.

Regulation of prostaglandin H synthase activity in dog urothelial cells

Results suggest that the late response with TPA is caused by de novo synthesis of prostaglandin H synthase, and primary and subcultured dog urothelial cells possess two distinct mechanisms for regulating signal transduction by arachidonic acid metabolism.

Arachidonic acid-dependent peroxidative activation of carcinogenic arylamines by extrahepatic human tissue microsomes.

To confirm the occurrence of PHS antigen in human extrahepatic tissues, an avidin/biotin-amplified competitive enzyme-linked immunoabsorbent assay was developed with purified ram PHS and a commercially available monoclonal antibody known to cross-react with human platelet PHS.

Regulation of PG Synthase by EGF and PDGF in Human Oral, Breast, Stomach, and Fibrosarcoma Cancer Cell Lines

The results suggest that EGF and PDGF may be involved in the regulation of the PG synthase activities of human oral, breast, stomach, and fibrosarcoma cancer cells.

Drug metabolizing enzyme activities in porcine urinary bladder epithelial cell cultures (PUBEC)

It is shown that cultured porcine urinary bladder epithelial cells maintain several enzyme activities required for the biotransformation of xenobiotics, and may provide a useful in vitro model for this target tissue.

An in vitro model of the urinary bladder: cultured porcine urinary bladder epithelial cells.

Lipoxygenase Protein Expression and Its Effect on Oxidative Stress Caused by Benzidine in Normal Human Urothelial Cell Lines

BZ can be activated by 5-LOX to produce ROS and oxidative stress, which may be associated with bladder cancer caused by BZ, and is probably the major LOX isozyme to co-oxidize exogenous chemicals in SV-HUC-1 cells.

Peroxygenase Metabolism of N-Acetylbenzidine by Prostaglandin H Synthase

The lack of effect of 5,5-dimethyl-1-pyrroline N-oxide, mannitol, andsuperoxide dismutase suggests the lack of involvement of one-electron transfer reactions and suggests that hydroxyl radicals and superoxide are not sources of oxygen or oxidants.

The thromboxane synthase and receptor signaling pathway in cancer: an emerging paradigm in cancer progression and metastasis

This review will focus on some of the more recent findings and advances with a significant emphasis on understanding the functional role of TXA2S and TP in cancer progression and metastasis.



Eicosanoid synthesis by rabbit hydronephrotic cortical interstitial cells in culture.

It is suggested that PGG2 and/or PGH2 that are released from these cells may be metabolized further by adjacent kidney cells or circulating blood elements to other eicosanoid products, thus increasing the diversity of eicOSanoids synthesized in the hydronephrotic kidney.

Inhibition by prostaglandin synthesis inhibitors of the induction of epidermal ornithine decarboxylase activity, the accumulation of prostaglandins, and tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate.

The findings that the application of indomethacin prior to TPA treatment inhibits the accumulation of prostaglandins, the induction of ODC activity, and the formation of skin papillomas suggest that TPA-induced O DC activity may be an important component of the mechanism of skin tumor promotion.

Arachidonic acid transformation and tumor production.

  • L. Levine
  • Biology
    Advances in cancer research
  • 1981

Physiological and Pharmacological Regulation of Prostaglandin and Leukotriene Production by Macrophages

The synthesis and secretion of prostaglandins and leukotrienes by mouse peritioneal macrophages is under several regulatory controls and can be regulated by certain antiinflammatory compounds.

The stimulations of arachidonic acid metabolism by recombinant murine interleukin 1 and tumor promoters or 1-oleoyl-2-acetyl-glycerol are synergistic.

OAG and TPA mimic the endogenous activator of protein kinase C, 1,2-diacylglycerol, and therefore IL 1 may amplify arachidonic acid metabolism during signal transmission processes.

Prostaglandins and cancer: a review of tumor initiation through tumor metastasis.

Prostaglandin E2 production by rabbit urinary bladder.

It is demonstrated that the rabbit bladder can synthesize PGE2 and that the P GE2- synthesizing systems of the transitional epithelium and outer layer of bladder may be distinct.

Effects of platelet-activating factor on the release of arachidonic acid and prostaglandins by rabbit iris smooth muscle. Inhibition by calcium channel antagonists.

This conclusion is supported by the findings that both the removal of arachidonate and formation of lysophosphatidylinositol, from phosphorus-based phospholipids in prelabelled irides by PAF occur concomitantly in a time-dependent manner and that Ca2+ is required for the agonist-induced release of arACHidonates and PGE2.