Oncotarget

Research Papers:

RhoGDIα suppresses self-renewal and tumorigenesis of glioma stem cells

Fan Wu, Peishan Hu, Dengke Li, Yan Hu, Yingjiao Qi, Bin Yin, Tao Jiang, Jiangang Yuan, Wei Han and Xiaozhong Peng _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:61619-61629. https://doi.org/10.18632/oncotarget.11423

Metrics: PDF 1922 views  |   HTML 2338 views  |   ?  


Abstract

Fan Wu1, Peishan Hu1, Dengke Li1, Yan Hu1, Yingjiao Qi1, Bin Yin1, Tao Jiang2, Jiangang Yuan1, Wei Han1, Xiaozhong Peng1

1State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China

2Department of Neurosurgery, Beijing Tiantan Hospital, Beijing 100050, China

Correspondence to:

Xiaozhong Peng, email: [email protected]

Wei Han, email: [email protected]

Keywords: GSCs, RhoGDIα, self-renewal, ROCK1, Oct4

Received: October 07, 2015     Accepted: August 08, 2016     Published: August 19, 2016

ABSTRACT

Glioma stem cells (GSCs) are a subset of tumor cells that drive glioma initiation and progression. The molecular mechanisms underlying the maintenance of GSCs are still poorly understood. Here we investigated the role of Rho GDP dissociation inhibitor α (RhoGDIα) in GSCs. RhoGDIα was down-regulated in glioma stem cells. Over-expression of RhoGDIα suppressed the self-renewal and tumorigenesis of GSCs. Further data showed that RhoGDIα inhibited the transcription activity of stem cell marker Oct4. Moreover, inactivation of ROCK1, a downstream effector of RhoGDIα, also decreased the self-renewal and Oct4 transcription activity, and rescued the effects caused by RhoGDIα knockdown. Our results indicate that RhoGDIα is involved in the maintenance of GSCs.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 11423