Sun Lihua, Zhang Chuanbao, Yang Zhengxiang, Wu Yiping, Wang Hongjun, Bao Zhaoshi, Jiang Tao
Department of Molecular Neuropathology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Department of Neurosurgery, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China.
Oncotarget. 2016 Apr 26;7(17):24646-55. doi: 10.18632/oncotarget.8261.
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.
驱动蛋白家族成员23（KIF23）是一种核蛋白，也是细胞胞质分裂的关键调节因子，已被发现在胶质瘤中作为癌基因过度表达。然而，KIF23表达的胶质瘤的预后及临床病理特征尚不清楚。在此，我们利用中国胶质瘤基因组图谱（CGGA）数据库（http://www.cgga.org.cn）中的全基因组mRNA表达微阵列数据，分析了KIF23的表达模式，发现在生存分析中（对数秩检验，p<0.01），KIF23的过度表达与高级别胶质瘤以及更高的死亡率显著相关。其他三个验证数据集的结果显示了相似的发现。此外，KIF23在胶质瘤患者中也是一个独立的预后生物标志物。最后，功能分析表明，KIF23的减少在体内和体外均抑制了胶质瘤细胞的增殖。此外，我们发现KIF23在转录水平上受TCF-4调控。因此，该证据表明KIF23的过表达与胶质瘤的恶性程度相关，并导致胶质瘤患者生存时间缩短，这表明KIF23是一种新的具有潜在治疗意义的预后生物标志物。
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