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.
Highlights
Glioma, the most common malignant neoplasm of central nervous system, remains one of the most lethal tumors for its refractory features to conventional therapies [1]
The traditional classification of glioma by WHO is based on histological morphology, and the same treatments were applied to the patients according to tumor grade [21]
Later research found that in proliferation cells, Kinesin family member 23 (KIF23) is essential for midbody formation and completion of cell cytokinesis, for which accumulates to the central antiparallel overlap zone of the microtubule-based structures and recruits various downstream cytokinesis factors to the site of division [14, 23, 24]
Summary
The most common malignant neoplasm of central nervous system, remains one of the most lethal tumors for its refractory features to conventional therapies [1]. The survival time of GBM patients, ranging from months to over 5 years following diagnosis [5]. This phenomenon may due to the heterogeneity of tumor, indicating the limitations of the current morphology based diagnosis, prediction and prognosis evaluation. The prognostic and molecular features of glioma with KIF23 expression is unknown, and the regulation mechanism of KIF23 is still unclear. We demonstrated that TCF-4 regulated KIF23 expression at transcriptional level. These results suggest KIF23 is a novel biomarker with potential important therapeutic implications in glioma
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