Thomas E Eling

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint NSAID activated gene (NAG-1), a modulator of tumorigenesis
    Thomas E Eling
    National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    J Biochem Mol Biol 39:649-55. 2006
  2. pmc The cyclooxygenase inhibitor sulindac sulfide inhibits EP4 expression and suppresses the growth of glioblastoma cells
    Atsushi Kambe
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Cancer Prev Res (Phila) 2:1088-99. 2009
  3. ncbi request reprint Expression of NAG-1, a transforming growth factor-beta superfamily member, by troglitazone requires the early growth response gene EGR-1
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 279:6883-92. 2004
  4. pmc Regulation of EP4 expression via the Sp-1 transcription factor: inhibition of expression by anti-cancer agents
    Atsushi Kambe
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina 27709, USA
    Biochim Biophys Acta 1783:1211-9. 2008
  5. ncbi request reprint The anti-invasive activity of cyclooxygenase inhibitors is regulated by the transcription factor ATF3 (activating transcription factor 3)
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, P O Box 12233, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cancer Ther 4:693-703. 2005
  6. ncbi request reprint Overexpression of 15-lipoxygenase-1 induces growth arrest through phosphorylation of p53 in human colorectal cancer cells
    Jong Sik Kim
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, MD, USA
    Mol Cancer Res 3:511-7. 2005
  7. ncbi request reprint Drug-induced expression of nonsteroidal anti-inflammatory drug-activated gene/macrophage inhibitory cytokine-1/prostate-derived factor, a putative tumor suppressor, inhibits tumor growth
    Jeanelle M Martinez
    Laboratories of Molecular Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    J Pharmacol Exp Ther 318:899-906. 2006
  8. ncbi request reprint Gene modulation by the cyclooxygenase inhibitor, sulindac sulfide, in human colorectal carcinoma cells: possible link to apoptosis
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, the Laboratory of Computational Biology and Risk Analysis, and National Center for Toxicogenomics, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 278:25790-801. 2003
  9. ncbi request reprint Transcriptional regulation of activating transcription factor 3 involves the early growth response-1 gene
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    J Pharmacol Exp Ther 315:668-77. 2005
  10. ncbi request reprint Cyclooxygenase inhibitors induce the expression of the tumor suppressor gene EGR-1, which results in the up-regulation of NAG-1, an antitumorigenic protein
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Pharmacol 67:356-64. 2005

Collaborators

Detail Information

Publications55

  1. ncbi request reprint NSAID activated gene (NAG-1), a modulator of tumorigenesis
    Thomas E Eling
    National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    J Biochem Mol Biol 39:649-55. 2006
    ..In addition, an increase in NAG-1 is observed in inhibition of the AKT/GSK-3beta pathway, suggesting NAG-1 alters cell survival. Thus, NAG-1 expression is regulated by tumor suppressor pathways and appears to modulate tumor progression...
  2. pmc The cyclooxygenase inhibitor sulindac sulfide inhibits EP4 expression and suppresses the growth of glioblastoma cells
    Atsushi Kambe
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Cancer Prev Res (Phila) 2:1088-99. 2009
    ..Our data suggest that the suppression of EP4 expression by sulindac sulfide represents a new mechanism for understanding the tumor suppressor activity...
  3. ncbi request reprint Expression of NAG-1, a transforming growth factor-beta superfamily member, by troglitazone requires the early growth response gene EGR-1
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 279:6883-92. 2004
    ..Our results suggest that EGR-1 induction is a unique property of TGZ, but is independent of PPARgamma activation. The up-regulation of NAG-1 may provide a novel explanation for the antitumorigenic property of TGZ...
  4. pmc Regulation of EP4 expression via the Sp-1 transcription factor: inhibition of expression by anti-cancer agents
    Atsushi Kambe
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina 27709, USA
    Biochim Biophys Acta 1783:1211-9. 2008
    ..Thus, we propose that the expression of EP4 is regulated by Sp-1, but phosphorylation of Sp-1 induced by TGZ suppresses this expression. This represents a new and unique mechanism for the regulation of the EP4 receptor expression...
  5. ncbi request reprint The anti-invasive activity of cyclooxygenase inhibitors is regulated by the transcription factor ATF3 (activating transcription factor 3)
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, P O Box 12233, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cancer Ther 4:693-703. 2005
    ..In conclusion, ATF3 represents a novel mechanism in which NSAIDs exert their anti-invasive activity, thereby linking ATF3 and its gene regulatory activity to the biological activity of these compounds...
  6. ncbi request reprint Overexpression of 15-lipoxygenase-1 induces growth arrest through phosphorylation of p53 in human colorectal cancer cells
    Jong Sik Kim
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, MD, USA
    Mol Cancer Res 3:511-7. 2005
    ....
  7. ncbi request reprint Drug-induced expression of nonsteroidal anti-inflammatory drug-activated gene/macrophage inhibitory cytokine-1/prostate-derived factor, a putative tumor suppressor, inhibits tumor growth
    Jeanelle M Martinez
    Laboratories of Molecular Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    J Pharmacol Exp Ther 318:899-906. 2006
    ..Drugs that target NAG-1 could lead to a unique strategy for the development of chemotherapeutic and chemopreventive agents...
  8. ncbi request reprint Gene modulation by the cyclooxygenase inhibitor, sulindac sulfide, in human colorectal carcinoma cells: possible link to apoptosis
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, the Laboratory of Computational Biology and Risk Analysis, and National Center for Toxicogenomics, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 278:25790-801. 2003
    ..In conclusion, this is the first report showing sulindac sulfide, independent of cyclooxygenase, altered the expression of several genes possibly linked to its anti-tumorigenic and pro-apoptotic activity...
  9. ncbi request reprint Transcriptional regulation of activating transcription factor 3 involves the early growth response-1 gene
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    J Pharmacol Exp Ther 315:668-77. 2005
    ..Therefore, this is a novel first report demonstrating that the expression of ATF3 occurs via Egr-1 downstream of Erk1/2...
  10. ncbi request reprint Cyclooxygenase inhibitors induce the expression of the tumor suppressor gene EGR-1, which results in the up-regulation of NAG-1, an antitumorigenic protein
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Pharmacol 67:356-64. 2005
    ..NAG-1 seems to be an important downstream target protein of this transcription factor, EGR-1, and may mediate the chemopreventive activity of some NSAIDs...
  11. pmc Vitamin E succinate induces NAG-1 expression in a p38 kinase-dependent mechanism
    Minsub Shim
    Eicosanoids Biochemistry Section, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cancer Ther 7:961-71. 2008
    ....
  12. ncbi request reprint The conventional nonsteroidal anti-inflammatory drug sulindac sulfide arrests ovarian cancer cell growth via the expression of NAG-1/MIC-1/GDF-15
    Jong Sik Kim
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, MD E4 09, P O Box 12233, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cancer Ther 4:487-93. 2005
    ..In conclusion, a novel molecular mechanism is proposed to explain the experimental results and provide a rationale for the chemopreventive activity of NSAIDs in ovarian cancer...
  13. ncbi request reprint The cyclooxygenase inhibitor indomethacin modulates gene expression and represses the extracellular matrix protein laminin gamma1 in human glioblastoma cells
    Minako Ishibashi
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    Exp Cell Res 302:244-52. 2005
    ..These findings are important in understanding the chemopreventive activity of some NSAIDs and could be relevant for designing therapeutic strategies against glioblastoma...
  14. ncbi request reprint Protein kinase C-dependent regulation of NAG-1/placental bone morphogenic protein/MIC-1 expression in LNCaP prostate carcinoma cells
    Minsub Shim
    Eicosanoids Biochemistry Section, Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 280:18636-42. 2005
    ..These results demonstrate that NAG-1 expression is up-regulated by TPA in LNCaP cells through a PKC-dependent pathway involving the activation of NF-kappa B...
  15. ncbi request reprint Curcumin suppresses interleukin 1beta-mediated microsomal prostaglandin E synthase 1 by altering early growth response gene 1 and other signaling pathways
    Yuseok Moon
    Eicosanoid Biochemistry Section, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    J Pharmacol Exp Ther 315:788-95. 2005
    ..These results indicate that curcumin inhibits IL-1beta-induced PGE(2) formation by inhibiting the expression of mPGES-1 that is mediated by suppression of EGR-1 expression as well as NF-kappaB and JNK1/2...
  16. ncbi request reprint Suppression of tumor cell invasion by cyclooxygenase inhibitors is mediated by thrombospondin-1 via the early growth response gene Egr-1
    Yuseok Moon
    Eicosanoid Biochemistry Section, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Mol Cancer Ther 4:1551-8. 2005
    ..This is the first report suggesting that COX inhibitors suppress tumor cell invasion via TSP-1, which occurs downstream of Egr-1...
  17. pmc Nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) expression is increased by the histone deacetylase inhibitor trichostatin A
    Hiroki Yoshioka
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 283:33129-37. 2008
    ..TSA also increases the stability of NAG-1 mRNA. TSA-induced NAG-1 expression involves multiple mechanisms at the transcriptional and post-transcriptional levels...
  18. pmc DNA methylation-mediated silencing of nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) in glioma cell lines
    Mitsutoshi Kadowaki
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Int J Cancer 130:267-77. 2012
    ..We concluded from these data that methylation of specific promoter sequences causes transcriptional silencing of the NAG-1 locus in glioma and may ultimately contribute to tumor progression...
  19. ncbi request reprint Selective nonsteroidal anti-inflammatory drugs induce thymosin beta-4 and alter actin cytoskeletal organization in human colorectal cancer cells
    Anshu K Jain
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA
    J Pharmacol Exp Ther 311:885-91. 2004
    ..These data suggest that NSAIDs alter the expression of a diverse number of genes and provide new insights into the chemopreventive and biological activity of these drugs...
  20. ncbi request reprint Troglitazone, a peroxisome proliferator-activated receptor gamma (PPAR gamma ) ligand, selectively induces the early growth response-1 gene independently of PPAR gamma. A novel mechanism for its anti-tumorigenic activity
    Seung Joon Baek
    Eicosanoids Biochemistry Section, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 278:5845-53. 2003
    ..Thus, the up-regulation of Egr-1 may provide an explanation for the anti-tumorigenic properties of TGZ...
  21. ncbi request reprint Gene modulation by Cox-1 and Cox-2 specific inhibitors in human colorectal carcinoma cancer cells
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Carcinogenesis 25:349-57. 2004
    ....
  22. doi request reprint A reciprocal relationship exists between non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) and cyclooxygenase-2
    Genzo Iguchi
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T W Alexander Drive, RTP, NC 27709, USA
    Cancer Lett 282:152-8. 2009
    ..Furthermore, PGE(2) reduces NAG-1 while celebrex induces NAG-1 expression. The results suggest that a possible inverse relationship exists between the expression of NAG-1 and COX-2 in tumor formation of colon tissue...
  23. ncbi request reprint EGR1 is a novel target for AhR agonists in human lung epithelial cells
    Jeanelle M Martinez
    Laboratory of Computational Biology and Risk Analysis, NIEHS, Research Triangle Park, North Carolina 27709, USA
    Toxicol Sci 82:429-35. 2004
    ..Increased expression of a transcription factor EGR1 with tumorigenic and other biological activities could contribute to the deleterious pulmonary effects of exposure to these environmental agents...
  24. ncbi request reprint 15-Lipoxygenase-1 has anti-tumorigenic effects in colorectal cancer
    Jennifer B Nixon
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, Research Triangle Park, NC 27709, USA
    Prostaglandins Leukot Essent Fatty Acids 70:7-15. 2004
    ..These data demonstrate that 13(S)-HODE induces changes in gene expression and has anti-tumorigenic effects...
  25. pmc The H6D variant of NAG-1/GDF15 inhibits prostate xenograft growth in vivo
    Xingya Wang
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, 111 T W Alexander Dr Research Triangle Park, North Carolina 27709, USA
    Prostate 72:677-89. 2012
    ..The objective of the current study is to investigate the activity of NAG-1 H6D variant in prostate cancer tumorigenesis in vivo...
  26. ncbi request reprint Nonsteroidal anti-inflammatory drug-activated gene (NAG-1) is induced by genistein through the expression of p53 in colorectal cancer cells
    Leigh C Wilson
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Int J Cancer 105:747-53. 2003
    ..Together our data suggest a relationship between genistein, p53 and NAG-1 forming a novel pathway responsible for the antitumorigenic activity of genistein...
  27. ncbi request reprint Modulation of cyclooxygenase-2 expression by APC in HT-29 human colorectal carcinoma cells
    Linda C Hsi
    National Institute of Environmental Health Sciences, Eicosanoid Biochemistry Section, Laboratory of Molecular Carcinogenesis, Research Triangle Park, NC 27709, USA
    Adv Exp Med Biol 507:127-31. 2002
  28. ncbi request reprint Dual function of nonsteroidal anti-inflammatory drugs (NSAIDs): inhibition of cyclooxygenase and induction of NSAID-activated gene
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA
    J Pharmacol Exp Ther 301:1126-31. 2002
    ..In conclusion, NSAIDs have dual function, induction of NAG-1 expression and inhibition of COX activity that occurs in a variety of cell lines...
  29. pmc Proteasome inhibitor MG132 induces NAG-1/GDF15 expression through the p38 MAPK pathway in glioblastoma cells
    Sachie Shimizu
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Biochem Biophys Res Commun 430:1277-82. 2013
    ..We propose that the induction of NAG-1 by p38 MAPK is a potential contributor to the anti-glioblastoma activity of proteasome inhibitors...
  30. ncbi request reprint Role of reactive oxygen species in LPS-induced production of prostaglandin E2 in microglia
    Tongguang Wang
    Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, North Carolina 27709, USA
    J Neurochem 88:939-47. 2004
    ..These findings suggest a potential therapeutic intervention strategy for the treatment of inflammation-mediated neurodegenerative diseases...
  31. ncbi request reprint Opposing effects of 15-lipoxygenase-1 and -2 metabolites on MAPK signaling in prostate. Alteration in peroxisome proliferator-activated receptor gamma
    Linda C Hsi
    Eicosanoid Biochemistry Section, Laboratory of Molecular Carcinogenesis, NIEHS National Institutes of Health, Research Triangle Park, NC 27709, USA
    J Biol Chem 277:40549-56. 2002
    ..These results provide a plausible mechanism to explain the apparent opposing effects 15-LOX-1 and 15-LOX-2 play in prostate cancer...
  32. pmc Identification and functional characterization of polymorphisms in human cyclooxygenase-1 (PTGS1)
    Craig R Lee
    Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Chapel Hill, North Carolina, USA
    Pharmacogenet Genomics 17:145-60. 2007
    ..We sought to identify and characterize the functional relevance of genetic polymorphisms in PTGS1...
  33. ncbi request reprint Expression and regulation of nonsteroidal anti-inflammatory drug-activated gene (NAG-1) in human and mouse tissue
    Kyung Su Kim
    Laboratories of Molecular Carcinogenesis, Experimental Pathology, and Environmental Carcinogenesis Mutagenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, USA
    Gastroenterology 122:1388-98. 2002
    ..However, NAG-1 expression and its relationship with apoptosis in human and mouse intestinal tract have not been determined...
  34. ncbi request reprint Diallyl disulfide (DADS) induces the antitumorigenic NSAID-activated gene (NAG-1) by a p53-dependent mechanism in human colorectal HCT 116 cells
    Frank G Bottone
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    J Nutr 132:773-8. 2002
    ..9-fold increase in apoptosis, respectively. In contrast, 23 micromol/L DADS induced apoptosis only 1.8-fold in HCT-15 cells and not at all in PC-3 cells. Thus, DADS-induced apoptosis and NAG-1 protein expression appear to occur via p53...
  35. doi request reprint The role of NAG-1/GDF15 in the inhibition of intestinal polyps in APC/Min mice by sulindac
    Xingya Wang
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina, USA
    Cancer Prev Res (Phila) 4:150-60. 2011
    ..Our study also suggests that pharmacologic properties should be carefully evaluated when developing drug candidates...
  36. pmc The diverse roles of nonsteroidal anti-inflammatory drug activated gene (NAG-1/GDF15) in cancer
    Xingya Wang
    Eicosanoid Biochemistry Group, Laboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC 27709, USA
    Biochem Pharmacol 85:597-606. 2013
    ....
  37. ncbi request reprint Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53
    Seung Joon Baek
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Carcinogenesis 23:425-34. 2002
    ..The data may provide linkage between p53, NAG-1 and resveratrol, and in part, a new clue to the molecular mechanism of the antitumorigenic activity of natural polyphenolic compounds...
  38. ncbi request reprint High levels of GDF15 in thalassemia suppress expression of the iron regulatory protein hepcidin
    Toshihiko Tanno
    Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Med 13:1096-101. 2007
    ..These results suggest that GDF15 overexpression arising from an expanded erythroid compartment contributes to iron overload in thalassemia syndromes by inhibiting hepcidin expression...
  39. ncbi request reprint Transcriptional regulation of cyclooxygenase-1 by histone deacetylase inhibitors in normal human astrocyte cells
    Seijiro Taniura
    Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 277:16823-30. 2002
    ..In conclusion, COX-1 is an inducible gene in glial-derived cells including immortalized cells, and appears to be transcriptionally regulated by a unique mechanism associated with histone acetylation...
  40. ncbi request reprint Arachidonic and linoleic acid metabolism in mouse intestinal tissue: evidence for novel lipoxygenase activity
    Hiroo Kawajiri
    Eicosanoid Biochemistry Section, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Arch Biochem Biophys 398:51-60. 2002
    ....
  41. pmc A green tea component suppresses posttranslational expression of basic fibroblast growth factor in colorectal cancer
    Mugdha Sukhthankar
    Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996, USA
    Gastroenterology 134:1972-80. 2008
    ..However, the exact molecular mechanism by which EGCG suppresses bFGF expression is not known. Our objective was to elucidate the molecular mechanisms by which EGCG inhibits bFGF expression in colorectal cancer...
  42. pmc A transcriptional signaling pathway in the IFN system mediated by 2'-5'-oligoadenylate activation of RNase L
    Krishnamurthy Malathi
    Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Proc Natl Acad Sci U S A 102:14533-8. 2005
    ..Because 2-5A and RNase L participate in defenses against viral infections and prostate cancer, our findings have implications for basic cellular mechanisms that control major pathogenic processes...
  43. ncbi request reprint Changes in gene expression contribute to cancer prevention by COX inhibitors
    Seung Joon Baek
    University of Tennessee, Department of Pathobiology, College of Veterinary Medicine Knoxville, TN 37996, USA
    Prog Lipid Res 45:1-16. 2006
    ....
  44. ncbi request reprint Nonsteroidal anti-inflammatory drug-activated gene-1 over expression in transgenic mice suppresses intestinal neoplasia
    Seung Joon Baek
    Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee, USA
    Gastroenterology 131:1553-60. 2006
    ..However, its antitumorigenic activity has not been elucidated in vivo...
  45. ncbi request reprint Aspirin and indomethacin exhibit antiproliferative effects and induce apoptosis in T98G human glioblastoma cells
    Ruhul Amin
    Department of Neurosurgery, Institute of Neurological Sciences, Faculty of Medicine, Tottori University School of Medicine, 36 1 Nishi cho, Yonago, Tottori 683 8504, Japan
    Neurol Res 25:370-6. 2003
    ..Our in vitro findings indicate that aspirin and indomethacin have an antiproliferative effect on T98G human glioblastoma cells at toxic concentrations...
  46. ncbi request reprint Functional genomic characterization of delipidation elicited by trans-10, cis-12-conjugated linoleic acid (t10c12-CLA) in a polygenic obese line of mice
    Ralph L House
    Department of Animal Science, North Carolina State University, Raleigh, North Carolina 27695, USA
    Physiol Genomics 21:351-61. 2005
    ..01). In conclusion, this experiment has revealed candidate genes that will be useful in elucidating mechanisms of adipose delipidation...
  47. ncbi request reprint Conjugated linoleic acid stimulates an anti-tumorigenic protein NAG-1 in an isomer specific manner
    Seong Ho Lee
    Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA
    Carcinogenesis 27:972-81. 2006
    ..The current study demonstrates that t10,c12-CLA stimulates ATF3/NAG-1 expression and subsequently induces apoptosis in an isomer specific manner. These effects may be through inhibition of AKT/GSK-3beta pathway in human CRC cells...
  48. ncbi request reprint Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells
    Seung Joon Baek
    Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA
    Carcinogenesis 25:2425-32. 2004
    ..The data generated by this study will help elucidate mechanisms of action for components in green tea and this information may lead to the design of more effective anticancer agents and informed clinical trials...
  49. ncbi request reprint A novel peroxisome proliferator-activated receptor gamma ligand, MCC-555, induces apoptosis via posttranscriptional regulation of NAG-1 in colorectal cancer cells
    Kiyoshi Yamaguchi
    Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA
    Mol Cancer Ther 5:1352-61. 2006
    ....
  50. ncbi request reprint The effect of 15-lipoxygenase-1 expression on cancer cells
    Uddhav Kelavkar
    Renal Division, Emory University, 4893 Farm Valley Drive, Atlanta, GA 30188, USA
    Curr Urol Rep 3:207-14. 2002
    ..This article is divided into three sections emphasizing the key role of 15-LO-1 in prostate, colorectal, and breast cancers...
  51. ncbi request reprint Prostate derived factor in human prostate cancer cells: gene induction by vitamin D via a p53-dependent mechanism and inhibition of prostate cancer cell growth
    James R Lambert
    Department of Pathology, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA
    J Cell Physiol 208:566-74. 2006
    ..These data demonstrate that PDF exerts antitumorigenic properties on PCa cells and its regulation by 1,25D may provide insights into the action of 1,25D in PCa...
  52. ncbi request reprint Identification of nonsteroidal anti-inflammatory drug-activated gene (NAG-1) as a novel downstream target of phosphatidylinositol 3-kinase/AKT/GSK-3beta pathway
    Kiyoshi Yamaguchi
    Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996, USA
    J Biol Chem 279:49617-23. 2004
    ..These data suggest that expression of NAG-1 is regulated by PI3K/AKT/GSK-3beta pathway in HCT-116 cells and may provide a further understanding of the important role of PI3K/AKT/GSK-3beta pathway in tumorigenesis...
  53. ncbi request reprint Indole-3-carbinol and 3,3'-diindolylmethane induce expression of NAG-1 in a p53-independent manner
    Seong Ho Lee
    Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA
    Biochem Biophys Res Commun 328:63-9. 2005
    ..Furthermore, the mixture of I3C with resveratrol enhances NAG-1 expression, suggesting the synergistic effect of these two unrelated compounds on NAG-1 expression...
  54. ncbi request reprint Cyclooxygenase inhibitors induce apoptosis in oral cavity cancer cells by increased expression of nonsteroidal anti-inflammatory drug-activated gene
    Kyung Su Kim
    Department of Otorhinolaryngology, Yonsei University College of Medicine, 134 Shinchon dong, Seodaemoon Gu, Seoul, Republic of Korea
    Biochem Biophys Res Commun 325:1298-303. 2004
    ..In summary, some NSAIDs induce NAG-1 expression in oral cavity cancer cells and the induced NAG-1 protein appears to mediate apoptosis. Therefore, NSAIDs may be considered as a possible chemopreventive agent against oral cavity cancer...
  55. pmc Growth compensatory role of sulindac sulfide-induced thrombospondin-1 linked with ERK1/2 and RhoA GTPase signaling pathways
    Yuseok Moon
    Department of Microbiology and Immunology and Medical Research Institute, Pusan National University School of Medicine, Busan, 602 739, Republic of Korea
    Life Sci 82:591-9. 2008
    ..These findings suggest the possible mechanism through which tumor cells can survive the chemopreventive action of NSAIDs or the normal epithelium can reconstitute after NSAID-mediated ulceration in a compensatory way...