SH3KBP1 Promotes Glioblastoma Tumorigenesis by Activating EGFR Signaling

Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. Overexpression or activation of epidermal growth factor receptor (EGFR) occurs commonly in multiple human cancers and promotes tumorigenesis. However, the underlying molecular mechanism of EGFR aberrant activation and the do...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in oncology 2021-02, Vol.10, p.583984-583984
Main Authors: Song, Hai, Wang, Yanpei, Shi, Chaojia, Lu, Jianxiang, Yuan, Tian, Wang, Xiangpeng
Format: Article
Language:English
Subjects:
adaptor
epidermal growth factor receptor
glioblastoma
glioblastoma stem cells
Oncology
SH3KBP1
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. Overexpression or activation of epidermal growth factor receptor (EGFR) occurs commonly in multiple human cancers and promotes tumorigenesis. However, the underlying molecular mechanism of EGFR aberrant activation and the downstream signaling pathways remains largely unknown. In this study, we report that both SH3-domain kinase binding protein 1 (SH3KBP1) mRNA and protein levels are highly expressed in GBM and its high expression is associated with worse survival of glioma patients. In addition, we provide evidence that SH3KBP1 is prominently expressed in GBM stem cells (GSCs) and have potential to serve as a novel GSCs marker. Moreover, silencing SH3KBP1 dramatically impairs GBM cell proliferation, migration and GSCs self-renewal ability and xenograft tumors growth . Most importantly, we found that SH3KBP1 directly interacts with EGFR and may act as an adaptor protein to transduce EGFR signaling. Together, our work uncovers SH3KBP1 as a novel regulator of oncogenic EGFR signaling and also as a potential therapeutic target for GBM patients with EGFR activation.
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2020.583984