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MET Signaling Regulates Glioblastoma Stem Cells

Authors
Joo, Kyeung MinJin, JuyounKim, EunheeKim, Kang HoKim, YonghyunKang, Bong GuKang, Youn-JungLathia, Justin D.Cheong, Kwang HoSong, Paul H.Kim, HyunggeeSeol, Ho JunKong, Doo-SikLee, Jung-IlRich, Jeremy N.Lee, JeongwuNam, Do-Hyun
Issue Date
1-8월-2012
Publisher
AMER ASSOC CANCER RESEARCH
Citation
CANCER RESEARCH, v.72, no.15, pp.3828 - 3838
Indexed
SCIE
SCOPUS
Journal Title
CANCER RESEARCH
Volume
72
Number
15
Start Page
3828
End Page
3838
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/107740
DOI
10.1158/0008-5472.CAN-11-3760
ISSN
0008-5472
Abstract
Glioblastomas multiforme (GBM) contain highly tumorigenic, self-renewing populations of stem/initiating cells [glioblastoma stem cells (GSC)] that contribute to tumor propagation and treatment resistance. However, our knowledge of the specific signaling pathways that regulate GSCs is limited. The MET tyrosine kinase is known to stimulate the survival, proliferation, and invasion of various cancers including GBM. Here, we identified a distinct fraction of cells expressing a high level of MET in human primary GBM specimens that were preferentially localized in perivascular regions of human GBM biopsy tissues and were found to be highly clonogenic, tumorigenic, and resistant to radiation. Inhibition of MET signaling in GSCs disrupted tumor growth and invasiveness both in vitro and in vivo, suggesting that MET activation is required for GSCs. Together, our findings indicate that MET activation in GBM is a functional requisite for the cancer stem cell phenotype and a promising therapeutic target. Cancer Res; 72(15); 3828-38. (C) 2012 AACR.
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