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15-Keto prostaglandin E2 induces heme oxygenase-1 expression through activation of Nrf2 in human colon epithelial CCD 841 CoN cells

DC Field Value Language
dc.contributor.authorLee, Jeong-Eun-
dc.contributor.authorZhong, Xiancai-
dc.contributor.authorLee, Ja-Young-
dc.contributor.authorSurh, Young-Joon-
dc.contributor.authorNa, Hye-Kyung-
dc.date.accessioned2021-01-31T09:19:22Z-
dc.date.available2021-01-31T09:19:22Z-
dc.date.created2020-04-06-
dc.date.created2020-04-06-
dc.date.issued2020-01-
dc.identifier.citationArchives of Biochemistry and Biophysics, Vol.679, p. 108162-
dc.identifier.issn0003-9861-
dc.identifier.other94848-
dc.identifier.urihttps://hdl.handle.net/10371/172570-
dc.description.abstractProstaglandin E-2 (PGE(2)) plays a key role in inflammation-associated carcinogenesis. NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of the 15(S)-hydroxyl group of PGE(2) to generate 15-keto PGE(2). 15-PGDH has been known as a tumor suppressor in various malignancies including colon cancer. However, the molecular mechanisms underlying the tumor-suppressive function of 15-PGDH remain largely unresolved. In this study, we found that 15-keto PGE(2) upregulated the expression of heme oxygenase-1 (HO-1), a representative antioxidative and anti-inflammatory enzyme, at both transcriptional and translational levels, in human colon epithelial CCD 841 CoN cells. A redox-sensitive transcription factor, NF-E2-related factor (Nrf2) plays a critical role in the regulation of HO-1 and other cytoprotective proteins. 15-Keto PGE(2) induced translocation of Nrf2 into the nucleus and antioxidant response element-driven luciferase activity. Furthermore, the silencing of the Nrf2 gene abolished 15-keto PGE(2)-induced HO-1 expression in CCD 841 CoN cells. 15-Keto PGE(2) activated AKT signaling, and the pharmacological AKT inhibitor, LY294002 suppressed the 15-keto PGE(2)-induced HO-1 expression. 15-Keto PGE(2) generates the reactive oxygen species which is suppressed by the general antioxidant N-acetyl-L-cysteine. N-acetyl-L-cysteine treatment attenuated the 15-keto PGE(2)-induced phosphorylation of GSK3 beta, transcriptional activity of Nrf2, and subsequently HO-1 expression. However, 13,14-dihydro-15-keto PGE(2) lacking the alpha,beta-unsaturated carbonyl moiety failed to induce intracellular production of reactive oxygen species, HO-1 expression and nuclear translocation of Nrf2. In conclusion, 15-keto PGE(2) induces HO-1 expression through Nrf2 activation in human colon epithelial cells.-
dc.language영어-
dc.publisherAcademic Press-
dc.title15-Keto prostaglandin E2 induces heme oxygenase-1 expression through activation of Nrf2 in human colon epithelial CCD 841 CoN cells-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1016/j.abb.2019.108162-
dc.citation.journaltitleArchives of Biochemistry and Biophysics-
dc.identifier.wosid000525443900002-
dc.identifier.scopusid2-s2.0-85076837756-
dc.citation.startpage108162-
dc.citation.volume679-
dc.identifier.sci000525443900002-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorSurh, Young-Joon-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlus15-HYDROXYPROSTAGLANDIN DEHYDROGENASE-
dc.subject.keywordPlusINCREASED SUSCEPTIBILITY-
dc.subject.keywordPlusDOWN-REGULATION-
dc.subject.keywordPlusOXIDANT STRESS-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusKEAP1-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusPROGNOSIS-
dc.subject.keywordPlusENZYMES-
dc.subject.keywordAuthor15-Keto PGE(2)-
dc.subject.keywordAuthorNrf2-
dc.subject.keywordAuthorHeme oxygenase-1-
dc.subject.keywordAuthorROS-
dc.subject.keywordAuthorColon-
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