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The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets
DC Field | Value | Language |
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dc.contributor.author | Na, Hye-Kyung | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2021-01-31T09:20:37Z | - |
dc.date.available | 2021-01-31T09:20:37Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2008-01 | - |
dc.identifier.citation | Asia Pacific Journal of Clinical Nutrition, Vol.17, pp.204-207 | - |
dc.identifier.issn | 0964-7058 | - |
dc.identifier.other | 3279 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172587 | - |
dc.description.abstract | We previously reported that a novel alkylphospholipid type antitumor agent edelfosine (ET-18-O-CH3; 1-O-octadecyl-2-O-methyl-glycero-3-phosphocholine) induced apoptosis in human breast epithelial cells transfected with the H-ras oncogene (MCF10A-ras) which was causally linked to cyclooxygenase-2 (COX-2) up-regulation and production of 15-deoxy-Delta(12,14)-prostaglandins J(2) (15d-PGJ2). ET-18-O-CH3 treatment also enhanced the production of prostaglandin E-2 (PGE(2)), a major COX-2 product. In this study, we found that ET-18-O-CH3 treatment resulted in elevated mRNA expression of the PGE2 receptor subunit, EP2 receptor. Exogenously added PGE2 inhibited the growth of MCF10A-ras cells and induced proteolytic cleavage of caspase 3. ET-18-O-CH3 also inhibited constitutive activation of ERK 1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635. In addition, ET-18-O-CH3 inhibited DNA binding activity of NF-kappa B in MCF10A-ras cells, and this was again attenuated by SC58635. Based on these findings, it is likely that ET-18-O-CH3 inactivates ERK1/2, Akt, and NF-kappa B signaling via COX-2 induction in MCF10A-ras cells, thereby inducing apoptosis of these cells. | - |
dc.language | 영어 | - |
dc.publisher | H E C Press | - |
dc.title | The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.citation.journaltitle | Asia Pacific Journal of Clinical Nutrition | - |
dc.identifier.wosid | 000254987900051 | - |
dc.identifier.scopusid | 2-s2.0-46049092032 | - |
dc.citation.endpage | 207 | - |
dc.citation.startpage | 204 | - |
dc.citation.volume | 17 | - |
dc.identifier.sci | 000254987900051 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article; Proceedings Paper | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | FACTOR-KAPPA-B | - |
dc.subject.keywordPlus | UP-REGULATION | - |
dc.subject.keywordPlus | CANCER-CELLS | - |
dc.subject.keywordPlus | BINDING PROTEIN | - |
dc.subject.keywordPlus | CYCLOOXYGENASE-2 | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | COX-2 | - |
dc.subject.keywordPlus | LINE | - |
dc.subject.keywordAuthor | ET-18-O-CH3 | - |
dc.subject.keywordAuthor | edelfosine | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | COX-2 | - |
dc.subject.keywordAuthor | MCF10A-ras cells | - |
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