title: Inhibition of ultraviolet B-induced AP-1 activation by theaflavins from black tea.
abstract: Theaflavins are believed to be key active components in black tea for chemoprevention of cancer. However, the molecular mechanisms underlying the inhibitory effects of theaflavins are not clear. With the JB6 mouse epidermal cell line, we investigated the effects of theaflavins on ultraviolet (UV) B radiation-induced activator protein-1 (AP-1)-dependent transcriptional activation and compared them with (-)-epigallocatechin-3-gallate (EGCG), a major green tea polyphenol that has cancer chemopreventative activity. Theaflavins and EGCG inhibited UVB-induced AP-1 activation in a concentration-dependent manner. The inhibitory effects of theaflavins were stronger than those of EGCG. We found that theaflavins significantly inhibited activation of extracellular signal-regulated protein kinases and c-jun NH(2)-terminal kinases. Because the transcription factor AP-1 is important in the process of tumor promotion, the inhibitory effect of these polyphenols on AP-1 activation may further explain the anti-tumor promotion action of these tea constituents. Mol. Carcinog. 28:148-155, 2000.
authors.affiliation: The Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA.
authors.forename: M
authors.initials: M
authors.lastname: Nomura
authors.forename: W Y
authors.initials: WY
authors.lastname: Ma
authors.forename: C
authors.initials: C
authors.lastname: Huang
authors.forename: C S
authors.initials: CS
authors.lastname: Yang
authors.forename: G T
authors.initials: GT
authors.lastname: Bowden
authors.forename: K
authors.initials: K
authors.lastname: Miyamoto
authors.forename: Z
authors.initials: Z
authors.lastname: Dong
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D044946:Biflavonoids; D002110:Caffeine / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002460:Cell Line; D003864:Depression, Chemical; D004789:Enzyme Activation / Q000187:drug effects / Q000528:radiation effects; D000078404:Epidermal Cells; D004817:Epidermis / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000528:radiation effects; D017930:Genes, Reporter; D008156:Luciferases / Q000096:biosynthesis / Q000235:genetics; D020935:MAP Kinase Signaling System / Q000187:drug effects* / Q000528:radiation effects; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects / Q000528:radiation effects; D011494:Protein Kinases / Q000378:metabolism; D011499:Protein Processing, Post-Translational / Q000187:drug effects / Q000528:radiation effects; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis; D013662:Tea / Q000737:chemistry*; D018808:Transcription Factor AP-1 / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects* / Q000528:radiation effects; D014162:Transfection; D014466:Ultraviolet Rays
chemical_list: D016588:Anticarcinogenic Agents; D044946:Biflavonoids; D011993:Recombinant Fusion Proteins; D013662:Tea; D018808:Transcription Factor AP-1; C056068:theaflavin; D002110:Caffeine; D002392:Catechin; C045651:epigallocatechin gallate; D008156:Luciferases; D011494:Protein Kinases