Peroxiredoxin I contributes to TRAIL resistance through suppression of redox-sensitive caspase activation in human hepatoma cells

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dc.contributor.authorIn-Seong Song-
dc.contributor.authorSun-Uk Kim-
dc.contributor.authorNang-Su Oh-
dc.contributor.authorJ Kim-
dc.contributor.authorDae Yeul Yu-
dc.contributor.authorS M Huang-
dc.contributor.authorJ M Kim-
dc.contributor.authorD S Lee-
dc.contributor.authorNam-Soon Kim-
dc.date.accessioned2017-04-19T09:14:08Z-
dc.date.available2017-04-19T09:14:08Z-
dc.date.issued2009-
dc.identifier.issn0143-3334-
dc.identifier.uri10.1093/carcin/bgp104ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9041-
dc.description.abstractReactive oxygen species (ROS) have been implicated in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance of many cancers. We evaluated the role of peroxiredoxin (Prx) I in TRAIL resistance governed by coupling of nicotinamide adenosine dinucleotide phosphate oxidase (Nox)-derived ROS signaling with the p38 mitogen-activated protein kinase (MAPK)/caspase-signaling cascade in liver cancer cells. Upregulated Prx I expression was found in neoplastic regions of human patient liver, and Prx I knockdown resulted in accelerated TRAIL-induced cell death in SK-Hep-1 human hepatoma cells. The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling. Furthermore, we found that Nox4 was constitutively expressed in both SK-Hep-1 cells and tumor regions of patient livers, knockdown of Nox4 expression could alleviate ROS generation and TRAIL-mediated cytotoxicity. In accordance with previous findings, increased activation of both p38 MAPK and caspase cascades by Prx I knockdown was inhibited by either Nox4 knockdown or SB203580 addition. Collectively, these data suggest that Prx I functions to block propagation of Nox-derived ROS signaling to the p38 MAPK/caspase/cell death cascade during TRAIL treatment and also provides a molecular mechanism by which Prx I contributes to TRAIL resistance in liver cancers.-
dc.publisherOxford Univ Press-
dc.titlePeroxiredoxin I contributes to TRAIL resistance through suppression of redox-sensitive caspase activation in human hepatoma cells-
dc.title.alternativePeroxiredoxin I contributes to TRAIL resistance through suppression of redox-sensitive caspase activation in human hepatoma cells-
dc.typeArticle-
dc.citation.titleCarcinogenesis-
dc.citation.number7-
dc.citation.endPage1114-
dc.citation.startPage1106-
dc.citation.volume30-
dc.contributor.affiliatedAuthorIn-Seong Song-
dc.contributor.affiliatedAuthorSun-Uk Kim-
dc.contributor.affiliatedAuthorNang-Su Oh-
dc.contributor.affiliatedAuthorDae Yeul Yu-
dc.contributor.affiliatedAuthorNam-Soon Kim-
dc.contributor.alternativeName송인성-
dc.contributor.alternativeName김선욱-
dc.contributor.alternativeName오낭수-
dc.contributor.alternativeName김지영-
dc.contributor.alternativeName유대열-
dc.contributor.alternativeNameHuang-
dc.contributor.alternativeName김진만-
dc.contributor.alternativeName이동석-
dc.contributor.alternativeName김남순-
dc.identifier.bibliographicCitationCarcinogenesis, vol. 30, no. 7, pp. 1106-1114-
dc.identifier.doi10.1093/carcin/bgp104-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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