title: The possible role of heat shock factor-1 in the negative regulation of heme oxygenase-1.
abstract: We examined a possible role for heat shock factor-1 (HSF-1) in the negative regulation of HO-1 gene expression in human Hep3B hepatoma cells responding to stimulation with 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) and arsenite. Overexpression of HSF-1 and heat-shock experiments indicated that HSF-1 repressed the 15d-PGJ2-and arsenite-induced HO-1 gene expression through directly binding to the consensus heat shock element (HSE) of the HO-1 gene promoter. In addition, point mutations at specific HSE sequences of the HO-1 promoter-driven luciferase plasmid (pGL2/hHO3.2-Luc) abolished the heat shock- and HSF-1-mediated repression of reporter activity. Overall, it is possible that HSF-1 negatively regulates HO-1 gene expression, and that the HSE present in the -389 to -362 region mediates HSF-1-induced repression of human HO-1 gene expression.
authors.affiliation: Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
authors.forename: Yenn-Hwei
authors.initials: YH
authors.lastname: Chou
authors.forename: Feng-Ming
authors.initials: FM
authors.lastname: Ho
authors.forename: Der-Zen
authors.initials: DZ
authors.lastname: Liu
authors.forename: Shyr-Yi
authors.initials: SY
authors.lastname: Lin
authors.forename: Li-Hsueh
authors.initials: LH
authors.lastname: Tsai
authors.forename: Chien-Ho
authors.initials: CH
authors.lastname: Chen
authors.forename: Yuan-Soon
authors.initials: YS
authors.lastname: Ho
authors.forename: Ling-Fang
authors.initials: LF
authors.lastname: Hung
authors.forename: Yu-Chih
authors.initials: YC
authors.lastname: Liang
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D018053:Arsenites / Q000494:pharmacology; D015153:Blotting, Western; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D004268:DNA-Binding Proteins / Q000502:physiology*; D024202:Electrophoretic Mobility Shift Assay; D004790:Enzyme Induction / Q000187:drug effects; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D017930:Genes, Reporter; D000076249:Heat Shock Transcription Factors; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis* / Q000235:genetics; D051547:Heme Oxygenase-1; D006801:Humans; D008156:Luciferases / Q000378:metabolism; D008565:Membrane Proteins; D016297:Mutagenesis, Site-Directed; D010957:Plasmids; D017354:Point Mutation; D011401:Promoter Regions, Genetic; D015230:Prostaglandin D2 / Q000031:analogs & derivatives* / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors; D015533:Transcriptional Activation
chemical_list: D000970:Antineoplastic Agents; D018053:Arsenites; D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; D008565:Membrane Proteins; D015534:Trans-Activators; D014157:Transcription Factors; C037112:9-deoxy-delta-9-prostaglandin D2; D008156:Luciferases; C496541:HMOX1 protein, human; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; C015001:arsenite; D015230:Prostaglandin D2