Oncotarget

Research Papers:

KIF23 is an independent prognostic biomarker in glioma, transcriptionally regulated by TCF-4

Lihua Sun _, Chuanbao Zhang, Zhengxiang Yang, Yiping Wu, Hongjun Wang, Zhaoshi Bao and Tao Jiang

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Oncotarget. 2016; 7:24646-24655. https://doi.org/10.18632/oncotarget.8261

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Abstract

Lihua Sun1,2,*, Chuanbao Zhang1,*, Zhengxiang Yang2, Yiping Wu2, Hongjun Wang3, Zhaoshi Bao4, Tao Jiang1,4,5,6

1Department of Molecular Neuropathology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

2Department of Neurosurgery, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi, China

3Department of Neurosurgery, 2nd Affiliated hospital of Harbin Medical University, Harbin, China

4Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

5Center of Brain Tumor, Beijing Institute for Brain Disorders, Beijing, China

6China National Clinical Research Center for Neurological Diseases, Beijing, China

*These authors have contributed equally to this work

Correspondence to:

Zhaoshi Bao, e-mail: [email protected]

Tao Jiang, e-mail: [email protected]

Keywords: glioma, prognostic, KIF23, TCF-4, proliferation

Received: December 06, 2015    Accepted: March 04, 2016    Published: March 22, 2016

ABSTRACT

Kinesin family member 23 (KIF23), a nuclear protein and a key regulator of cellular cytokinesis, has been found to be overexpressed as an oncogene in glioma. However, the prognostic and clinicopathological features of glioma with KIF23 expression was not clear yet. Here, we analyzed KIF23 expression pattern by using whole genome mRNA expression microarray data from Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn), and found that KIF23 overexpression was significantly associated with high grade glioma as well as the higher mortality in survival analysis (log-rank test, p<0.01). The results of the three other validation datasets showed similar findings. Furthermore, KIF23 also served as an independent prognostic biomarker in glioma patients. Finally, functional assay showed that reduction of KIF23 suppressed glioma cell proliferation both in vivo and vitro. Additionally, we found that KIF23 was regulated by TCF-4 at transcriptionally level. Therefore, this evidence indicates KIF23 over-expression is associated with glioma malignancy and conferred a worse survival time in glioma, which suggests KIF23 is a new novel prognostic biomarker with potential therapeutic implications in glioma.


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