Affiliation: University of Utah
- JS-K, a nitric oxide prodrug, has enhanced cytotoxicity in colon cancer cells with knockdown of thioredoxin reductase 1Kornelia Edes
Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America
PLoS ONE 5:e8786. 2010..Therefore, a greater understanding of the role of thioredoxin reductase in redox initiated apoptotic processes is warranted...
- Transcriptional responses of human aortic endothelial cells to nanoconstructs used in biomedical applicationsPhilip J Moos
Department of Pharmacology and Toxicology, Utah Center for Nanomedicine, Nano Institute of Utah, University of Utah, Salt Lake City, Utah 84112, United States
Mol Pharm 10:3242-52. 2013..However, the dendrimers did not induce genomic toxicity, despite displaying general cytotoxicity. ..
- Responses of human cells to ZnO nanoparticles: a gene transcription studyPhilip J Moos
Department of Pharmacology and Toxicology, University of Utah, 30 S 2000 East, Salt Lake City, Utah 84112, USA
Metallomics 3:1199-211. 2011..This provides some of the first data on the effects of commercial metal oxide nanoparticles on human colon-derived and skin-derived cells...
- ZnO particulate matter requires cell contact for toxicity in human colon cancer cellsPhilip J Moos
Department of Pharmacology and Toxicology, University of Utah, L S Skaggs Pharmacy, Room 201, 30 S 2000 East, Salt Lake City, Utah 84112, USA
Chem Res Toxicol 23:733-9. 2010..Both ZnO samples induced similar mechanisms of toxicity, but there was a statistically significant increase in potency per unit mass with the smaller particles...
- Pre- and post-initiation chemoprevention activity of 2-alkyl/aryl selenazolidine-4(R)-carboxylic acids against tobacco-derived nitrosamine (NNK)-induced lung tumors in the A/J mouseMichael R Franklin
University of Utah, Department of Pharmacology and Toxicology, Salt Lake City, UT 84112, USA
Chem Biol Interact 168:211-20. 2007..Thus, several 2-aryl/alkyl selenazolidines possess chemopreventive activity against NNK-induced lung tumors, and variously demonstrate pre-initiation and post-initiation efficacy...
- Curcumin impairs tumor suppressor p53 function in colon cancer cellsPhilip J Moos
Department of Oncological Sciences and Department of Medicinal Chemistry, University of Utah, Huntsman Cancer Institute, Salt Lake City, UT 84112, USA
Carcinogenesis 25:1611-7. 2004..It disrupts the conformation of the p53 protein required for its serine phosphorylation, its binding to DNA, its transactivation of p53-responsive genes and p53-mediated cell cycle arrest...
- Thioredoxin reductase 1 knockdown enhances selenazolidine cytotoxicity in human lung cancer cells via mitochondrial dysfunctionRobyn L Poerschke
Department of Pharmacology and Toxicology, University of Utah, L S Skaggs Pharmacy, Room 201, 30 S 2000 East, Salt Lake City, UT 84112, USA
Biochem Pharmacol 81:211-21. 2011..These results indicate the ability of TR1 to modulate the cytotoxic effects of BSCA, ChSCA and SECY in human lung cancer cells through mitochondrial dysfunction...
- Thioredoxin reductase 1 ablation sensitizes colon cancer cells to methylseleninate-mediated cytotoxicityMatthew Honeggar
Department of Pharmacology and Toxicology, University of Utah, L S Skaggs Pharmacy, Rm 201, 30 S 2000 East, Salt Lake City, UT 84112, USA
Toxicol Appl Pharmacol 241:348-55. 2009..Therefore, the use of selenocompounds with anticancer activity, like MSA, might be utilized most effectively with agents that targets TR1 in chemotherapeutic applications...
- Identification of gene expression profiles that segregate patients with childhood leukemiaPhilip J Moos
Center for Children at the Huntsman Cancer Institute and Oncological Sciences, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
Clin Cancer Res 8:3118-30. 2002....
- Electrophilic prostaglandins and lipid aldehydes repress redox-sensitive transcription factors p53 and hypoxia-inducible factor by impairing the selenoprotein thioredoxin reductasePhilip J Moos
Huntsman Cancer Institute and Departments of Oncological Science and Medicinal Chemistry, University of Utah, Salt Lake City 84112 5550, USA
J Biol Chem 278:745-50. 2003....
- Modulation of redox status in human lung cell lines by organoselenocompounds: selenazolidines, selenomethionine, and methylseleninic acidRobyn L Poerschke
Department of Pharmacology and Toxicology, University of Utah, L S Skagg s Pharmacy, Rm 201, 30 S 2000 East, Salt Lake City, UT 84112, United States
Toxicol In Vitro 22:1761-7. 2008..These data demonstrate that all selenocompounds are not equal and that the form of the organic selenocompound is a major determinant in the expected cellular response...
- Thioredoxin reductase is required for the inactivation of tumor suppressor p53 and for apoptosis induced by endogenous electrophilesPamela B Cassidy
Huntsman Cancer Institute, The Department of Medicinal Chemistry, University of Utah, L S Skagg s Pharmacy, Room 201, 30 S 2000 Salt Lake City, UT 84112, USA
Carcinogenesis 27:2538-49. 2006..Endogenous lipid electrophiles have been our primary focus; however, metabolic activation of hormones can generate endogenous mutagens, and we demonstrate that estrone-quinone attenuates p53 function in human MCF7 cells...
- Differential gene expression in primary human skin keratinocytes and fibroblasts in response to ionizing radiationRaymond L Warters
Department of Radiation Oncology, University of Utah Health Sciences Center, Salt Lake City, Utah 84132, USA
Radiat Res 172:82-95. 2009..Both Q-PCR and Western blot analysis experiments validated these transcription changes. Our results are consistent with changes in the expression of p53 target genes as indicating the magnitude of cell responses to ionizing radiation...
- Oxidation of 2-Cys-peroxiredoxins by arachidonic acid peroxide metabolites of lipoxygenases and cyclooxygenase-2Pauline Cordray
Department of Pharmacology and Toxicology, and Huntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT 84112, USA
J Biol Chem 282:32623-9. 2007..A., Poole, L. B, and Karplus P. A. (2003) Science 300, 600-653). Peroxiredoxin-dependent mechanisms may modulate the receptor-dependent actions of autocoids derived from cellular lipoxygenase and cyclooxygenase catalysis...
- Transient receptor potential vanilloid 1 agonists cause endoplasmic reticulum stress and cell death in human lung cellsKaren C Thomas
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA
J Pharmacol Exp Ther 321:830-8. 2007..These findings are significant within the context of lung inflammatory diseases where elevated concentrations of endogenous TRPV1 agonists are probably produced in sufficient quantities to cause TRPV1 activation and lung cell death...
- Impact of microarray technology in clinical oncologyElizabeth A Raetz
Division of Hematology Oncology, Huntsman Cancer Institute, University of Utah School of Medicine, Primary Children s Medical Center, Salt Lake City, Utah, USA
Cancer Invest 22:312-20. 2004..The dynamic nature of this field ensures that new developments are missing from this review...
- Conditional expression of 15-lipoxygenase-1 inhibits the selenoenzyme thioredoxin reductase: modulation of selenoproteins by lipoxygenase enzymesMargaret K Yu
Department of Internal Medicine, The Huntsman Cancer Institute, University of Utah Health Sciences, Salt Lake City, UT 84112 0555, USA
J Biol Chem 279:28028-35. 2004..The influences of 15-lipoxygenase-1 on (1)inflammation, cell growth, and survival may be attributable, in part, to inhibition of thioredoxin reductase and several redox-sensitive processes subordinate to thioredoxin reductase...
- Cyclooxygenase-2 induction by paclitaxel, docetaxel, and taxane analogues in human monocytes and murine macrophages: structure-activity relationships and their implicationsPamela B Cassidy
Department of Medicinal Chemistry, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112 5550, USA
Clin Cancer Res 8:846-55. 2002..Binding at a second, lower-affinity receptor site is also necessary. However, our structure activity data are not fully compatible with two candidate proteins currently proposed as the low-affinity receptor...
- The role of selenoproteins in the etiology of cancerPhilip Moos; Fiscal Year: 2008..Does SelP have a novel function in the regulation of lipid hydroperoxides? These studies provide an integrated framework to understand how electrophiles and selenium/selenoproteins contribute to the etiology of cancer. ..