HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Institute for Genetic Medicine >
Peer-reviewed Journal Articles, etc >

Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway

Files in This Item:
Ohtsu_et_al-final_manuscript.pdf3.62 MBPDFView/Open
Ohtsu_et_al-revised-Supplementary_information.pdfSupplementary Information4.47 MBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway
Other Titles: Eva1 is a novel GIC regulator
Authors: Ohtsu, Naoki Browse this author
Nakatani, Yuka Browse this author
Yamashita, Daisuke Browse this author
Ohue, Shiro Browse this author →KAKEN DB
Ohnishi, Takanori Browse this author
Kondo, Toru Browse this author →KAKEN DB
Keywords: Glioblastoma (GBM)
GBM-initiating cells (GICs)
non-canonical NF-κB
Issue Date: Jan-2016
Publisher: American Association for Cancer Research
Journal Title: Cancer research
Volume: 76
Issue: 1
Start Page: 171
End Page: 181
Publisher DOI: 10.1158/0008-5472.CAN-15-0884
PMID: 26677976
Abstract: Glioblastoma (GBM)-initiating cells (GICs) are a tumorigenic subpopulation that are resistant to radio- and chemotherapies and are the source of disease recurrence. Therefore, the identification and characterization of GIC-specific factors is critical towards the generation of effective GBM therapeutics. In this study, we investigated the role of Epithelial V-like antigen 1 (Eva1, also known as myelin-like protein Zero like-2) in stemness and GBM tumorigenesis. Eva1 was prominently expressed in GICs in vitro and in stem cell marker (Sox2, CD15, CD49f)-expressing cells derived from human GBM tissues. Eva1 knockdown in GICs reduced their self-renewal and tumor-forming capabilities, whereas Eva1 overexpression enhanced these properties. Eva1-deficiency was also associated with decreased expression of stemness-related genes, indicating a requirement for Eva1 in maintaining GIC pluripotency. We further demonstrate that Eva1 induced GIC proliferation through the activation of the RelB-dependent noncanonical NF-κB pathway by recruiting TRAF2 to the cytoplasmic tail. Taken together, our findings highlight Eva1 as a novel regulator of GIC function and also provide new mechanistic insight into the role of non-canonical NF-κB activation in GIC, thus offering multiple potential therapeutic targets for preclinical investigation in GBM.
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 近藤 亨

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 - Hokkaido University