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Crosstalk between Glioma-Initiating Cells and Endothelial Cells Drives Tumor Progression

Authors
Jeon, Hye-MinKim, Sung-HakJin, XunPark, Jong BaeKim, Se HoonJoshi, KaushalNakano, IchiroKim, Hyunggee
Issue Date
16-8월-2014
Publisher
AMER ASSOC CANCER RESEARCH
Citation
CANCER RESEARCH, v.74, no.16, pp.4482 - 4492
Indexed
SCIE
SCOPUS
Journal Title
CANCER RESEARCH
Volume
74
Number
16
Start Page
4482
End Page
4492
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/97676
DOI
10.1158/0008-5472.CAN-13-1597
ISSN
0008-5472
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.
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