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Global gene expression of canine bladder K9TCC cells and cancer stem cells after COX-2 inhibition

ABSTRACT: Global gene expression of canine bladder K9TCC cells and cancer stem cells after COX-2 inhibition

PROVIDER: PRJNA762021 | ENA |

REPOSITORIES: ENA

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Global gene expression of canine bladder K9TCC cells and cancer stem cells after COX-2 inhibition

Project description:Cancer stem cells (CSCs) are fundamental to bladder cancer progression and the cyclooxygenase-2 (COX-2) pathway has a pro-tumorigenic role in CSC function. Naturally occurring bladder cancer in dogs has the potential to be a natural model of the human disease. Here, we used canine specific microarrays to determine changes in global gene expression of canine bladder cancer cells (the K9TCC cell line) and bladder cancer stem cells isolated from the K9TCC cell line after treatment with the selective COX-2 inhibitor mavacoxib or a COX-2 siRNA.

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Comparative gene expression analyses identify luminal and basal subtypes of canine invasive urothelial carcinoma that mimic patterns in human invasive bladder cancer

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Naturally-occurring canine invasive urothelial carcinoma harbors luminal and basal transcriptional subtypes found in human muscle invasive bladder cancer

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Activity-dependent COX-2 proteolysis

Project description:Cyclooxygenase-2 (COX-2) catalyzes the oxidation of arachidonic acid (AA) into a single product that is the source of all prostaglandins (PGs), ligands of multiple pro-inflammatory pathways. AA catalysis results in suicide inactivation, rendering the enzyme catalytically inactive. We report that catalytic activity also leads to controlled cleavage of COX-2, an event that is differentially regulated by fatty acids, and blocked by COX inhibitors. Using mass spectrometry, we identified two adjacent cleavage points within the catalytic domain, which give rise to COX-2 fragments that are catalytically inactive and localize to different cellular compartments. These fragments were also detected in human colon tumors. Expression of one of these fragments in cells significantly reduced mitochondrial function, increased lactate production, and enhanced proliferation.

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Expression data from Cerebral Cortex or Hippocampus of COX-1 or COX-2 null mice

Project description:To further understand the physiological role of cyclooxygenase (COX), the critical enzyme involved in the production of eicosanoids from arachidonic acid, we performed microarray analysis of gene expression in the cerebral cortex and hippocampus of mice deficient in COX-1 (COX-1-/-) or COX-2 (COX-2-/-). Expression of lipid (ATP citrate lyase, acetyl-CoA acetyltransferase, hydroxyacyl-CoA dehydrogenase) and homocysteine (methionine adenosyltransferase, S-adenosylhomocysteine hydrolase) metabolism genes was increased in the cerebral cortex of COX-2 -/- mice. Further, expression of GABAergic neurotransmission genes (GABA transporter 3, GABA-A receptor subunit ?1) was altered in the cerebral cortex and hippocampus of COX-2 -/- mice. A COX isoform specific effect was observed in the expression of Janus Kinase (JAK) 1 and 2. COX-1 -/- mice exhibited an increase in JAK1 expression while COX-2 -/- mice exhibited a decrease in JAK2 expression, an observation consistent with a previously demonstrated COX isoform specific effect on the expression of NF-kB. In summary, this study demonstrates the wide ranging effects of genetic deletion of COX isoforms in the mouse brain and suggests that inhibition of COX activity may alter the profile of gene expression in specific areas of the brain. We used nylon cDNA microarrays to detail the global programme of gene expression in the Cerebral Cortex and Hippocampus of COX-1 and COX-2 null (knockout) mice Keywords: brain, cerebral cortex, hippocampus, COX-1 WT, COX-1 KO, COX-2 WT, COX-2 KO and COX-2 heterozygous

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Inhibition of mPGES-1 or COX-2 Results in Different Proteomic and Lipidomic Profiles in A549 Lung Cancer Cells

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Opposing Effects of Cyclooxygenase-2 (COX-2) on Estrogen Receptor Î² (ERÎ²) Response to 5Î±-reductase Inhibition in Prostate Epithelial Cells

Project description:Current pharmacotherapies for symptomatic benign prostatic hyperplasia (BPH), an androgen receptor (AR) driven, inflammatory disorder affecting elderly men, include 5Î±-reductase (5AR) inhibitors (i.e. dutasteride and finasteride) to block the conversion of testosterone to the more potent AR ligand dihydrotestosterone (DHT). Since DHT is the precursor for estrogen receptor Î² (ERÎ²) ligands, 5AR inhibitors could potentially limit ERÎ² activation, which maintains prostate tissue homeostasis. We have uncovered signaling pathways in BPH-derived prostate epithelial cells (BPH-1) that are impacted by 5AR inhibition. The induction of apoptosis and repression of the cell-adhesion protein E-cadherin by the 5AR inhibitor, dutasteride, requires both ERÎ² and TGFÎ². Dutasteride also induces cyclooxygenase type 2 (COX-2), which functions in a negative-feedback loop in TGFÎ² and ERÎ² signaling pathways as evidenced by the potentiation of apoptosis induced by dutasteride or finasteride upon pharmacological inhibition or shRNA-mediated ablation of COX-2. Concurrently, COX-2 positively impacts ERÎ² action through its effect on the expression of a number of steroidogenic enzymes in the ERÎ²-ligand metabolic pathway. Therefore, effective combination pharmacotherapies, which have included non-steroidal anti-inflammatory drugs, must take into account biochemical pathways affected by 5AR inhibition and opposing effects of COX-2 on the tissue protective action of ERÎ². Next-generation sequencing (n=3) of shRNA mediated knockdown of COX-2 or scrambled control in BPH-1 prostate epithelial cell line

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