Research Papers:

Targeting dual specificity protein kinase TTK attenuates tumorigenesis of glioblastoma

Jia Wang, Yuchen Xie, Xiaobin Bai, Ning Wang, Hai Yu, Zhong Deng, Minxue Lian, Shuo Yu, Hao Liu, Wanfu Xie _ and Maode Wang

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2018; 9:3081-3088. https://doi.org/10.18632/oncotarget.23152

Metrics: PDF 1589 views  |   HTML 2579 views  |   ?  


Jia Wang1, Yuchen Xie2, Xiaobin Bai1, Ning Wang1, Hai Yu1,2, Zhong Deng1,2, Minxue Lian1, Shuo Yu2, Hao Liu1, Wanfu Xie1 and Maode Wang1

1Department of Neurosurgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi 710061, China

2School of Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi 710061, China

Correspondence to:

Wanfu Xie, email: [email protected]

Maode Wang, email: [email protected]

Keywords: glioma stem-like cells; glioblastoma; TTK; MTFR2

Received: June 15, 2017     Accepted: November 21, 2017     Published: December 11, 2017


Accumulating evidence has proved that glioma stem-like cells (GSCs) are responsible for tumorigenesis, treatment resistance, and subsequent tumor recurrence in glioblastoma (GBM). In this study, we identified dual specificity protein kinase TTK (TTK) as the most up-regulated and differentially expressed kinase encoding genes in GSCs. Functionally, TTK was essential for in vitro clonogenicity and in vivo tumor propagation in GSCs. Clinically, TTK expression was highly enriched in GBM, moreover, was inversely correlated with a poor prognosis in GBM patients. Mechanistically, mitochondrial fission regulator 2 (MTFR2) was identified as one of the most correlated genes to TTK and transcriptionally regulated TTK expression via activation of TTK promoter. Collectively, MTFR2-dependent regulation of TTK plays a key role in maintaining GSCs in GBM and is a potential novel druggable target for GBM.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 23152