The anti-inflammatory and anti-cancer properties of epigallocatechin-3-gallate are mediated by folate cycle disruption, adenosine release and NF-κB suppression

[1]  R. McCarley,et al.  Adenosine, prolonged wakefulness, and A1-activated NF-κB DNA binding in the basal forebrain of the rat , 2001, Neuroscience.

[2]  E M Schwarz,et al.  Rel/NF-kappa B/I kappa B family: intimate tales of association and dissociation. , 1995, Genes & development.

[3]  W. Shih,et al.  Inhibition of intestinal tumorigenesis in Apcmin/+ mice by (-)-epigallocatechin-3-gallate, the major catechin in green tea. , 2005, Cancer research.

[4]  B. Ludviksson,et al.  The anti-inflammatory action of methotrexate is not mediated by lymphocyte apoptosis, but by the suppression of activation and adhesion molecules. , 2005, Clinical immunology.

[5]  Insu P. Lee,et al.  Anticancer effects of (-)-epigallocatechin-3-gallate on ovarian carcinoma cell lines. , 2004, Gynecologic oncology.

[6]  D. Barrett,et al.  Methotrexate induced differentiation in colon cancer cells is primarily due to purine deprivation , 2006, Journal of cellular biochemistry.

[7]  Zuo-Feng Zhang,et al.  Green tea drinking and multigenetic index on the risk of stomach cancer in a Chinese population , 2005, International journal of cancer.

[8]  P. Roach,et al.  The antifolate activity of tea catechins. , 2005, Cancer research.

[9]  S. Wolffram,et al.  Inhibition of folic acid uptake by catechins and tea extracts in Caco-2 cells. , 2006, Planta medica.

[10]  M. Alic.  Green Tea for Remission Maintenance in Crohn's Disease? , 1999, American Journal of Gastroenterology.

[11]  D. Barros,et al.  Methotrexate as a preferential cyclooxygenase 2 inhibitor in whole blood of patients with rheumatoid arthritis. , 2000, Rheumatology.

[12]  D. Gingras,et al.  Green tea: prevention and treatment of cancer by nutraceuticals , 2004, The Lancet.

[13]  F. García-Cánovas,et al.  Kinetics of the inhibition of bovine liver dihydrofolate reductase by tea catechins: origin of slow-binding inhibition and pH studies. , 2005, Biochemistry.

[14]  B. Aggarwal.  Nuclear factor-κ B : The enemy within , 2004 .

[15]  Liang-LiangYu,et al.  Nuclear factor-κB p65 （RelA） transcription factor is constitutively activated in human colorectal carcinoma tissue , 2004 .

[16]  S. Gupta,et al.  Green tea polyphenol epigallocatechin-3-gallate differentially modulates nuclear factor kappaB in cancer cells versus normal cells. , 2000, Archives of biochemistry and biophysics.

[17]  H. Koh,et al.  Cyclic AMP Inhibits Akt Activity by Blocking the Membrane Localization of PDK1* , 2001, The Journal of Biological Chemistry.

[18]  P. Fishman,et al.  Methotrexate enhances the anti-inflammatory effect of CF101 via up-regulation of the A3 adenosine receptor expression , 2006, Arthritis research & therapy.

[19]  E M Berman,et al.  The renewed potential for folate antagonists in contemporary cancer chemotherapy. , 1991, Journal of medicinal chemistry.

[20]  R. Straub,et al.  Anti-inflammatory mechanisms of methotrexate in rheumatoid arthritis , 2001, Annals of the rheumatic diseases.

[21]  M. Seitz,et al.  Molecular and cellular effects of methotrexate. , 1999, Current opinion in rheumatology.

[22]  R. Robbins,et al.  Methotrexate inhibition of inducible nitric oxide synthase in murine lung epithelial cells in vitro. , 1998, American journal of respiratory cell and molecular biology.

[23]  Jen-kun Lin,et al.  (−)-Epigallocatechin-3-gallate Blocks the Induction of Nitric Oxide Synthase by Down-Regulating Lipopolysaccharide-Induced Activity of Transcription Factor Nuclear Factor-κB , 1997 .

[24]  G. Yang,et al.  Mechanisms of inhibition of carcinogenesis by tea. , 2000, BioFactors.

[25]  P. Fishman,et al.  An agonist to the A3 adenosine receptor inhibits colon carcinoma growth in mice via modulation of GSK-3β and NF-κB , 2004, Oncogene.

[26]  S. Bao,et al.  The activation of Akt/PKB signaling pathway and cell survival , 2005, Journal of cellular and molecular medicine.

[27]  Y. Ben-Neriah,et al.  NF-κB functions as a tumour promoter in inflammation-associated cancer , 2004, Nature.

[28]  U. Moens,et al.  The cAMP signalling pathway activates CREB through PKA, p38 and MSK1 in NIH 3T3 cells. , 2005, Cellular signalling.

[29]  Ximing Xu,et al.  Nuclear factor-kappaB p65 (RelA) transcription factor is constitutively activated in human colorectal carcinoma tissue. , 2004, World journal of gastroenterology.

[30]  J. Linden.  Molecular approach to adenosine receptors: receptor-mediated mechanisms of tissue protection. , 2001, Annual review of pharmacology and toxicology.

[31]  González-Yanes Carmen,et al.  Signalling mechanisms regulating lipolysis. , 2006, Cellular signalling.

[32]  Cheorl-Ho Kim,et al.  Epigallocatechin-3-gallate causes the p21/WAF1-mediated G1-phase arrest of cell cycle and inhibits matrix metalloproteinase-9 expression in TNF-α-induced vascular smooth muscle cells , 2005 .

[33]  L. Coussens,et al.  Cancer: An inflammatory link , 2004, Nature.

[34]  B. Aggarwal,et al.  Methotrexate Suppresses NF-κB Activation Through Inhibition of IκBα Phosphorylation and Degradation1 , 2001, The Journal of Immunology.

[35]  H. Fujiki,et al.  A New Function of Green Tea: Prevention of Lifestyle‐related Diseases , 2001, Annals of the New York Academy of Sciences.

[36]  V. Adhami,et al.  Green tea constituent epigallocatechin‐3‐gallate selectively inhibits COX‐2 without affecting COX‐1 expression in human prostate carcinoma cells , 2005, International journal of cancer.