PPARδ Is an APC-Regulated Target of Nonsteroidal Anti-Inflammatory Drugs

[1]  D. Ahnen,et al.  Colon cancer prevention by NSAIDs: what is the mechanism of action? , 2003, The European journal of surgery. Supplement. : = Acta chirurgica. Supplement.

[2]  R. Langenbach,et al.  Malignant Transformation and Antineoplastic Actions of Nonsteroidal Antiinflammatory Drugs (Nsaids) on Cyclooxygenase-Null Embryo Fibroblasts , 1999, The Journal of experimental medicine.

[3]  V. Steele,et al.  Chemopreventive efficacy of sulindac sulfone against colon cancer depends on time of administration during carcinogenic process. , 1999, Cancer research.

[4]  J. Morrow,et al.  Cyclo-oxygenase-2-derived prostacyclin mediates embryo implantation in the mouse via PPARdelta. , 1999, Genes & development.

[5]  B. Spiegelman,et al.  Loss-of-Function Mutations in PPARγ Associated with Human Colon Cancer , 1999 .

[6]  Frank McCormick,et al.  β-Catenin regulates expression of cyclin D1 in colon carcinoma cells , 1999, Nature.

[7]  J. Vane,et al.  Induction of an acetaminophen-sensitive cyclooxygenase with reduced sensitivity to nonsteroid antiinflammatory drugs. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[8]  L. Matrisian,et al.  Differential expression of matrilysin and cyclooxygenase‐2 in intestinal and colorectal neoplasms , 1999, Molecular carcinogenesis.

[9]  W F Bodmer,et al.  Target genes of beta-catenin-T cell-factor/lymphoid-enhancer-factor signaling in human colorectal carcinomas. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[10]  D. Botstein,et al.  WISP genes are members of the connective tissue growth factor family that are up-regulated in wnt-1-transformed cells and aberrantly expressed in human colon tumors. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[11]  S. Skinner,et al.  Sulindac inhibits colorectal tumour growth, but not prostaglandin synthesis in the rat , 1998, Journal of gastroenterology and hepatology.

[12]  Rajnish A. Gupta,et al.  Activation of PPARγ leads to inhibition of anchorage-independent growth of human colorectal cancer cells , 1998 .

[13]  A. Sparks,et al.  Identification of c-MYC as a target of the APC pathway. , 1998, Science.

[14]  Samuel Singer,et al.  Differentiation and reversal of malignant changes in colon cancer through PPARγ , 1998, Nature Medicine.

[15]  J. G. Alvarez,et al.  Activators of the nuclear receptor PPARγ enhance colon polyp formation , 1998, Nature Medicine.

[16]  K. Kinzler,et al.  Human Smad3 and Smad4 are sequence-specific transcription activators. , 1998, Molecular cell.

[17]  K. Kinzler,et al.  Mechanisms underlying nonsteroidal antiinflammatory drug-mediated apoptosis. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[18]  W. Wahli,et al.  DNA Binding Properties of Peroxisome Proliferator-activated Receptor Subtypes on Various Natural Peroxisome Proliferator Response Elements , 1997, The Journal of Biological Chemistry.

[19]  C. Paraskeva,et al.  Induction of apoptotic cell death in human colorectal carcinoma cell lines by a cyclooxygenase-2 (COX-2)-selective nonsteroidal anti-inflammatory drug: independence from COX-2 protein expression. , 1997, Clinical cancer research : an official journal of the American Association for Cancer Research.

[20]  D. Alberts,et al.  Sulindac sulfone inhibits azoxymethane-induced colon carcinogenesis in rats without reducing prostaglandin levels. , 1997, Cancer research.

[21]  Peter J. Brown,et al.  Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors α and γ , 1997 .

[22]  Barry M. Forman,et al.  Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors α and δ , 1997 .

[23]  K. Kinzler,et al.  Constitutive Transcriptional Activation by a β-Catenin-Tcf Complex in APC−/− Colon Carcinoma , 1997, Science.

[24]  Hans Clevers,et al.  Activation of β-Catenin-Tcf Signaling in Colon Cancer by Mutations in β-Catenin or APC , 1997, Science.

[25]  Paul Polakis,et al.  Stabilization of β-Catenin by Genetic Defects in Melanoma Cell Lines , 1997, Science.

[26]  J. Lehmann,et al.  Peroxisome Proliferator-activated Receptors α and γ Are Activated by Indomethacin and Other Non-steroidal Anti-inflammatory Drugs* , 1997, The Journal of Biological Chemistry.

[27]  Bruno C. Hancock,et al.  Suppression of Intestinal Polyposis in Apc Δ716 Knockout Mice by Inhibition of Cyclooxygenase 2 (COX-2) , 1996, Cell.

[28]  Raymond L. White,et al.  Self-Promotion? Intimate Connections Between APC and Prostaglandin H Synthase-2 , 1996, Cell.

[29]  K. Kinzler,et al.  Lessons from Hereditary Colorectal Cancer , 1996, Cell.

[30]  Michael Kühl,et al.  Functional interaction of β-catenin with the transcription factor LEF-1 , 1996, Nature.

[31]  Hans Clevers,et al.  XTcf-3 Transcription Factor Mediates β-Catenin-Induced Axis Formation in Xenopus Embryos , 1996, Cell.

[32]  B. Rigas,et al.  Effects of nonsteroidal anti-inflammatory drugs on proliferation and on induction of apoptosis in colon cancer cells by a prostaglandin-independent pathway. , 1996, Biochemical pharmacology.

[33]  K. Kinzler,et al.  Apoptosis and APC in colorectal tumorigenesis. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[34]  Philippe Kastner,et al.  Nonsteroid nuclear receptors: What Are genetic studies telling us about their role in real life? , 1995, Cell.

[35]  K. Umesono,et al.  The nuclear receptor superfamily: The second decade , 1995, Cell.

[36]  R. DuBois,et al.  Alterations in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxide synthase 2 , 1995, Cell.

[37]  Kai Yu,et al.  Differential Activation of Peroxisome Proliferator-activated Receptors by Eicosanoids (*) , 1995, The Journal of Biological Chemistry.

[38]  M. Kondo,et al.  Expression of cyclooxygenase-1 and -2 in human colorectal cancer. , 1995, Cancer research.

[39]  D. Alberts,et al.  Antineoplastic drugs sulindac sulfide and sulfone inhibit cell growth by inducing apoptosis. , 1995, Cancer research.

[40]  B. Rigas,et al.  Sulindac sulfide, an aspirin-like compound, inhibits proliferation, causes cell cycle quiescence, and induces apoptosis in HT-29 colon adenocarcinoma cells. , 1995, The Journal of clinical investigation.

[41]  Arthur M Buchberg,et al.  The secretory phospholipase A2 gene is a candidate for the Mom1 locus, a major modifier of ApcMin -induced intestinal neoplasia , 1995, Cell.

[42]  P. Polakis,et al.  Regulation of intracellular beta-catenin levels by the adenomatous polyposis coli (APC) tumor-suppressor protein. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[43]  R. Mukherjee,et al.  The Human Peroxisome Proliferator-activated Receptor (PPAR) Subtype NUC1 Represses the Activation of hPPARα and Thyroid Hormone Receptors (*) , 1995, The Journal of Biological Chemistry.

[44]  G. Ailhaud,et al.  Cloning of a Protein That Mediates Transcriptional Effects of Fatty Acids in Preadipocytes , 1995, The Journal of Biological Chemistry.

[45]  R. Coffey,et al.  Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. , 1994, Gastroenterology.

[46]  K. Kinzler,et al.  Association of the APC tumor suppressor protein with catenins. , 1993, Science.

[47]  F. Masiarz,et al.  Association of the APC gene product with beta-catenin. , 1993, Science.

[48]  E. Lander,et al.  Genetic identification of Mom-1, a major modifier locus affecting Min-induced intestinal neoplasia in the mouse , 1993, Cell.

[49]  A. Mahfoudi,et al.  Fatty acids and retinoids control lipid metabolism through activation of peroxisome proliferator-activated receptor-retinoid X receptor heterodimers. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[50]  J. Gustafsson,et al.  Interaction of the peroxisome-proliferator-activated receptor and retinoid X receptor. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[51]  G. Rodan,et al.  Identification of a new member of the steroid hormone receptor superfamily that is activated by a peroxisome proliferator and fatty acids. , 1992, Molecular endocrinology.

[52]  I. Issemann,et al.  The mouse peroxisome proliferator activated receptor recognizes a response element in the 5′ flanking sequence of the rat acyl CoA oxidase gene. , 1992, The EMBO journal.

[53]  G A Colditz,et al.  Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. , 1990, The New England journal of medicine.

[54]  B. Mollet,et al.  A Functional Interaction , 2001 .

[55]  J. V. Vanden Heuvel.  Peroxisome proliferator-activated receptors: a critical link among fatty acids, gene expression and carcinogenesis. , 1999, The Journal of nutrition.

[56]  K. Kinzler,et al.  A simplified system for generating recombinant adenoviruses. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[57]  M. Bertagnolli,et al.  The sulfide metabolite of sulindac prevents tumors and restores enterocyte apoptosis in a murine model of familial adenomatous polyposis. , 1998, Carcinogenesis.

[58]  J. Auwerx,et al.  Activation of the peroxisome proliferator-activated receptor γ promotes the development of colon tumors in C57BL/6J-APCMin/+ mice , 1998, Nature Medicine.

[59]  R. DuBois,et al.  Colorectal cancer and nonsteroidal anti-inflammatory drugs. , 1997, Advances in pharmacology.

[60]  M. Thun.  Aspirin and gastrointestinal cancer. , 1997, Advances in experimental medicine and biology.

[61]  W. Wahli,et al.  Peroxisome proliferator-activated receptors: a nuclear receptor signaling pathway in lipid physiology. , 1996, Annual review of cell and developmental biology.

[62]  T. Westfall,et al.  ALTERATIONS IN THE , 1985 .