Glioma-derived cancer stem cells are hypersensitive to proteasomal inhibition
DC Field | Value | Language |
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dc.contributor.author | Yoo, Young Dong | - |
dc.contributor.author | Lee, Dae-Hee | - |
dc.contributor.author | Cha-Molstad, Hyunjoo | - |
dc.contributor.author | Kim, Hyungsin | - |
dc.contributor.author | Mun, Su Ran | - |
dc.contributor.author | Ji, Changhoon | - |
dc.contributor.author | Park, Seong Hye | - |
dc.contributor.author | Sung, Ki Sa | - |
dc.contributor.author | Choi, Seung Ah | - |
dc.contributor.author | Hwang, Joonsung | - |
dc.contributor.author | Park, Deric M. | - |
dc.contributor.author | Kim, Seung-Ki | - |
dc.contributor.author | Park, Kyung-Jae | - |
dc.contributor.author | Kang, Shin-Hyuk | - |
dc.contributor.author | Oh, Sang Cheul | - |
dc.contributor.author | Ciechanover, Aaron | - |
dc.contributor.author | Lee, Yong J. | - |
dc.contributor.author | Kim, Bo Yeon | - |
dc.contributor.author | Kwon, Yong Tae | - |
dc.date.accessioned | 2021-09-03T11:12:13Z | - |
dc.date.available | 2021-09-03T11:12:13Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2017-01 | - |
dc.identifier.issn | 1469-221X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/84982 | - |
dc.description.abstract | Although proteasome inhibitors (PIs) are used as anticancer drugs to treat various cancers, their relative therapeutic efficacy on stem cells vs. bulk cancers remains unknown. Here, we show that stem cells derived from gliomas, GSCs, are up to 1,000-fold more sensitive to PIs (IC50, 27-70 nM) compared with their differentiated controls (IC50, 47 to >> 100 mu M). The stemness of GSCs correlates to increased ubiquitination, whose misregulation readily triggers apoptosis. PI-induced apoptosis of GSCs is independent of NF-jB but involves the phosphorylation of c-Jun N-terminal kinase as well as the transcriptional activation of endoplasmic reticulum (ER) stress-associated proapoptotic mediators. In contrast to the general notion that ER stress-associated apoptosis is signaled by prolonged unfolded protein response (UPR), GSC-selective apoptosis is instead counteracted by the UPR. ATF3 is a key mediator in GSC-selective apoptosis. Pharmaceutical uncoupling of the UPR from its downstream apoptosis sensitizes GSCs to PIs in vitro and during tumorigenesis in mice. Thus, a combinational treatment of a PI with an inhibitor of UPR-coupled apoptosis may enhance targeting of stem cells in gliomas. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | END RULE PATHWAY | - |
dc.subject | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject | TRAIL-INDUCED APOPTOSIS | - |
dc.subject | RECEPTOR 5 EXPRESSION | - |
dc.subject | GLIOBLASTOMA-MULTIFORME | - |
dc.subject | ER STRESS | - |
dc.subject | GROWTH ARREST | - |
dc.subject | BORTEZOMIB | - |
dc.subject | DEATH | - |
dc.subject | PS-341 | - |
dc.title | Glioma-derived cancer stem cells are hypersensitive to proteasomal inhibition | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Dae-Hee | - |
dc.contributor.affiliatedAuthor | Park, Kyung-Jae | - |
dc.contributor.affiliatedAuthor | Kang, Shin-Hyuk | - |
dc.contributor.affiliatedAuthor | Oh, Sang Cheul | - |
dc.identifier.doi | 10.15252/embr.201642360 | - |
dc.identifier.scopusid | 2-s2.0-85006983243 | - |
dc.identifier.wosid | 000392430400018 | - |
dc.identifier.bibliographicCitation | EMBO REPORTS, v.18, no.1, pp.150 - 168 | - |
dc.relation.isPartOf | EMBO REPORTS | - |
dc.citation.title | EMBO REPORTS | - |
dc.citation.volume | 18 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 150 | - |
dc.citation.endPage | 168 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | END RULE PATHWAY | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | TRAIL-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | RECEPTOR 5 EXPRESSION | - |
dc.subject.keywordPlus | GLIOBLASTOMA-MULTIFORME | - |
dc.subject.keywordPlus | ER STRESS | - |
dc.subject.keywordPlus | GROWTH ARREST | - |
dc.subject.keywordPlus | BORTEZOMIB | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | PS-341 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | c-Jun N-terminal kinase | - |
dc.subject.keywordAuthor | glioma stem cells | - |
dc.subject.keywordAuthor | proteasome inhibitors | - |
dc.subject.keywordAuthor | ubiquitin proteasome system | - |
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