Crosstalk between Glioma-Initiating Cells and Endothelial Cells Drives Tumor Progression
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jeon, Hye-Min | - |
dc.contributor.author | Kim, Sung-Hak | - |
dc.contributor.author | Jin, Xun | - |
dc.contributor.author | Park, Jong Bae | - |
dc.contributor.author | Kim, Se Hoon | - |
dc.contributor.author | Joshi, Kaushal | - |
dc.contributor.author | Nakano, Ichiro | - |
dc.contributor.author | Kim, Hyunggee | - |
dc.date.accessioned | 2021-09-05T06:07:43Z | - |
dc.date.available | 2021-09-05T06:07:43Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-08-16 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/97676 | - |
dc.description.abstract | Glioma-initiating cells (GIC), which reside within the perivascular microenvironment to maintain self-renewal capacity, are responsible for glioblastoma initiation, progression, and recurrence. However, the molecular mechanisms controlling crosstalk between GICs and endothelial cells are poorly understood. Here, we report that, in both GICs and endothelial cells, platelet-derived growth factor (PDGF)-driven activation of nitric oxide (NO) synthase increases NO-dependent inhibitor of differentiation 4 (ID4) expression, which in turn promotes JAGGED1-NOTCH activity through suppression of miR129 that specifically represses JAGGED1 suppression. This signaling axis promotes tumor progression along with increased GIC self-renewal and growth of tumor vasculature in the xenograft tumors, which is dramatically suppressed by NOTCH inhibitor. ID4 levels correlate positively with NOS2 (NO synthase-2), HES1, and HEY1 and negatively with miR129 in primary GICs. Thus, targeting the PDGF-NOS-ID4-miR129 axis and NOTCH activity in the perivascular microenvironment might serve as an efficacious therapeutic modality for glioblastoma. (C)2014 AACR. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER ASSOC CANCER RESEARCH | - |
dc.subject | NEURAL STEM-CELLS | - |
dc.subject | SELF-RENEWAL | - |
dc.subject | MALIGNANT GLIOMAS | - |
dc.subject | NOTCH LIGANDS | - |
dc.subject | BRAIN-TUMORS | - |
dc.subject | IN-VIVO | - |
dc.subject | PDGF-B | - |
dc.subject | ANGIOGENESIS | - |
dc.subject | GROWTH | - |
dc.subject | ACTIVATION | - |
dc.title | Crosstalk between Glioma-Initiating Cells and Endothelial Cells Drives Tumor Progression | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Jeon, Hye-Min | - |
dc.contributor.affiliatedAuthor | Kim, Hyunggee | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-13-1597 | - |
dc.identifier.scopusid | 2-s2.0-84905984393 | - |
dc.identifier.wosid | 000341186700026 | - |
dc.identifier.bibliographicCitation | CANCER RESEARCH, v.74, no.16, pp.4482 - 4492 | - |
dc.relation.isPartOf | CANCER RESEARCH | - |
dc.citation.title | CANCER RESEARCH | - |
dc.citation.volume | 74 | - |
dc.citation.number | 16 | - |
dc.citation.startPage | 4482 | - |
dc.citation.endPage | 4492 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | NEURAL STEM-CELLS | - |
dc.subject.keywordPlus | SELF-RENEWAL | - |
dc.subject.keywordPlus | MALIGNANT GLIOMAS | - |
dc.subject.keywordPlus | NOTCH LIGANDS | - |
dc.subject.keywordPlus | BRAIN-TUMORS | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | PDGF-B | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | ACTIVATION | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.