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An IκBα phosphorylation inhibitor induces heme oxygenase-1(HO-1) expression through the activation of reactive oxygen species (ROS)-Nrf2-ARE signaling and ROS-PI3K/Akt signaling in an NF-κB-independent mechanism
DC Field | Value | Language |
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dc.contributor.author | Min, KJ | - |
dc.contributor.author | Lee, JT | - |
dc.contributor.author | Joe, EH | - |
dc.contributor.author | Kwon, TK | - |
dc.date.accessioned | 2012-03-29 | - |
dc.date.available | 2012-03-29 | - |
dc.date.issued | 2011 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.uri | http://repository.ajou.ac.kr/handle/201003/6352 | - |
dc.description.abstract | Reactive oxygen species (ROS) are important signaling molecules in cells. Excessive ROS induce expression of inflammatory mediators, such as iNOS and COX2. Antioxidant enzymes, such as, heme oxygenase-1 (HO-1), tightly regulate ROS levels within cells. Here, we show that Bay 11-7082 (Bay) increased HO-1 mRNA and protein expression in human colon cancer HT29 cells. Bay induced translocation of NF-E2-related factor 2 (Nrf2) into nuclei and increased the binding activity of the antioxidant response element (ARE). In addition, PI3K/Akt inhibitor (LY294002) blocked Bay-induced HO-1 expression. Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt. However, PI3K/Akt signaling was independent of Bay-induced Nrf2 translocation and ARE binding activity. Furthermore, other NF-κB inhibitors, such as pyrrolidine dithiocarbamate (PDTC) and MG132, also increased HO-1 mRNA and protein expression. However, although overexpression of dominant negative inhibitory κB (IκB) reduced NF-κB-driven transcriptional activity, IκB overexpression did not increase HO-1 expression. Taken together, our results suggest that in human colon cancer HT29 cells, Bay induces HO-1 expression by increasing ROS production in an Nrf2-ARE and PI3K dependent manner, but Bay acts independently of NF-κB. | - |
dc.language.iso | en | - |
dc.subject.MESH | Analysis of Variance | - |
dc.subject.MESH | Electrophoretic Mobility Shift Assay | - |
dc.subject.MESH | Gene Expression Regulation | - |
dc.subject.MESH | Glutathione | - |
dc.subject.MESH | HT29 Cells | - |
dc.subject.MESH | Heme Oxygenase-1 | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Immunohistochemistry | - |
dc.subject.MESH | Leupeptins | - |
dc.subject.MESH | NF-E2-Related Factor 2 | - |
dc.subject.MESH | NF-kappa B | - |
dc.subject.MESH | Nitriles | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases | - |
dc.subject.MESH | Phosphorylation | - |
dc.subject.MESH | Proline | - |
dc.subject.MESH | Proto-Oncogene Proteins c-akt | - |
dc.subject.MESH | RNA, Messenger | - |
dc.subject.MESH | Reactive Oxygen Species | - |
dc.subject.MESH | Response Elements | - |
dc.subject.MESH | Signal Transduction | - |
dc.subject.MESH | Sulfones | - |
dc.subject.MESH | Thiocarbamates | - |
dc.subject.MESH | Transfection | - |
dc.title | An IκBα phosphorylation inhibitor induces heme oxygenase-1(HO-1) expression through the activation of reactive oxygen species (ROS)-Nrf2-ARE signaling and ROS-PI3K/Akt signaling in an NF-κB-independent mechanism | - |
dc.type | Article | - |
dc.identifier.pmid | 21620964 | - |
dc.identifier.url | http://linkinghub.elsevier.com/retrieve/pii/S0898-6568(11)00150-1 | - |
dc.contributor.affiliatedAuthor | 조, 은혜 | - |
dc.type.local | Journal Papers | - |
dc.identifier.doi | 10.1016/j.cellsig.2011.05.013 | - |
dc.citation.title | Cellular signalling | - |
dc.citation.volume | 23 | - |
dc.citation.number | 9 | - |
dc.citation.date | 2011 | - |
dc.citation.startPage | 1505 | - |
dc.citation.endPage | 1513 | - |
dc.identifier.bibliographicCitation | Cellular signalling, 23(9). : 1505-1513, 2011 | - |
dc.identifier.eissn | 1873-3913 | - |
dc.relation.journalid | J008986568 | - |
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