期刊
ONCOTARGET
卷 7, 期 43, 页码 69173-69187出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12507
关键词
NF-kappa B; glioblastoma; cancer stem cells; tumor-initiating cells
资金
- NIH [R35 CA194687]
- Accelerate Brain Cancer Cure
Glioblastoma multiforme (GBM) carries a poor prognosis and continues to lack effective treatments. Glioblastoma stem cells (GSCs) drive tumor formation, invasion, and drug resistance and, as such, are the focus of studies to identify new therapies for disease control. Here, we identify the involvement of IKK and NF-kappa B signaling in the maintenance of GSCs. Inhibition of this pathway impairs self-renewal as analyzed in tumorsphere formation and GBM expansion as analyzed in brain slice culture. Interestingly, both the canonical and non-canonical branches of the NF-kappa B pathway are shown to contribute to this phenotype. One source of NF-kappa B activation in GBM involves the TGF-beta/TAK1 signaling axis. Together, our results demonstrate a role for the NF-kappa B pathway in GSCs and provide a mechanistic basis for its potential as a therapeutic target in glioblastoma.
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