Oncotarget

Research Papers:

ER stress inducer tunicamycin suppresses the self-renewal of glioma-initiating cell partly through inhibiting Sox2 translation

Yang Xing, Yuqing Ge, Chanjuan Liu, Xiaobiao Zhang, Jianhai Jiang and Yuanyan Wei _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:36395-36406. https://doi.org/10.18632/oncotarget.8954

Metrics: PDF 1681 views  |   HTML 2412 views  |   ?  


Abstract

Yang Xing1,*, Yuqing Ge1,*, Chanjuan Liu1,*, Xiaobiao Zhang2, Jianhai Jiang1, Yuanyan Wei1

1Key Laboratory of Glycoconjuates Research, Ministry of Public Health, Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai, People’s Republic of China

2Division of Neurosurgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China

*These authors have contributed equally to this work

Correspondence to:

Yuanyan Wei, e-mail: [email protected]

Jianhai Jiang, e-mail: [email protected]

Xiaobiao Zhang, e-mail: [email protected]

Keywords: glioma-initiating cell, tunicamycin, Sox2, self-renewal

Received: December 02, 2015     Accepted: April 11, 2016     Published: April 23, 2016

ABSTRACT

Glioma-initiating cells possess tumor-initiating potential and are relatively resistant to conventional chemotherapy and irradiation. Therefore, their elimination is an essential factor for the development of efficient therapy. Here, we report that endoplasmic reticulum (ER) stress inducer tunicamycin inhibits glioma-initiating cell self-renewal as determined by neurosphere formation assay. Moreover, tunicamycin decreases the efficiency of glioma-initiating cell to initiate tumor formation. Although tunicamycin induces glioma-initiating cell apoptosis, apoptosis inhibitor z-VAD-fmk only partly abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin. Indeed, tunicamycin reduces the expression of self-renewal regulator Sox2 at translation level. Overexpression of Sox2 obviously abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin. Taken together, tunicamycin suppresses the self-renewal and tumorigenic potential of glioma-initiating cell partly through reducing Sox2 translation. This finding provides a cue to potential effective treatment of glioblastoma through controlling stem cells.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 8954