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KIF3C is associated with favorable prognosis in glioma patients and may be regulated by PI3K/AKT/mTOR pathway.
Journal of Neuro-Oncology ( IF 3.9 ) Pub Date : 2020-02-04 , DOI: 10.1007/s11060-020-03399-7
Yang Gao 1 , Liangdong Li 1 , Hui Zheng 2 , Changshuai Zhou 1 , Xin Chen 1 , Bin Hao 1 , Yiqun Cao 1
Affiliation  

PURPOSE Glioma is the most common malignant primary tumor in the central nervous system (CNS). KIF3C, a motor protein of the kinesin superfamily, is highly expressed in the CNS. Although KIF3C has been identified as a potential therapeutic target in malignant cancers, the expression and function of KIF3C in glioma remains unclear. METHODS The clinical characteristics of 53 patients with graded glioma (WHO I-IV) were analyzed in this study. The expression of KIF3C in glioma was evaluated by immunohistochemistry (IHC). Survival analysis was compared between higher and lower KIF3C expression groups. Data regarding the expression of KIF3C and survival analysis were also confirmed using the database from The Cancer Genome Atlas (TCGA). The potential mechanism of the regulation of tumor growth by KIF3C was investigated by an analysis of the public database from Oncomine. RESULTS Expression of the KIF3C protein was higher in the low-grade glioma (LGG) group (n = 20) than that in the high-grade glioma (HGG) group (n = 33) (P < 0.05). Glioma patients with higher expression of KIF3C had longer survival time (P < 0.05). The subgroup analysis showed that higher KIF3C expression predicted longer survival time in the LGG group (P < 0.05). These clinical results were consistent with those in the TCGA database. Bioinformatics analysis showed that the KIF3C mRNA expression was upregulated significantly in response to PI3K/AKT/mTOR pathway inhibition. CONCLUSION This study demonstrated that KIF3C might inhibit glioma growth to prolong survival time by regulating the PI3K/AKT/mTOR pathway, providing a potential therapeutic target in glioma.

中文翻译:

KIF3C与神经胶质瘤患者的良好预后相关,可能受PI3K / AKT / mTOR通路的调节。

目的胶质瘤是中枢神经系统(CNS)中最常见的恶性原发肿瘤。KIF3C是驱动蛋白超家族的运动蛋白,在CNS中高度表达。尽管已将KIF3C确定为恶性肿瘤的潜在治疗靶标,但仍不清楚KIF3C在神经胶质瘤中的表达和功能。方法对53例分级脑胶质瘤(WHO I-IV)患者的临床特征进行分析。通过免疫组织化学(IHC)评估了KIF3C在神经胶质瘤中的表达。比较较高和较低KIF3C表达组之间的生存分析。还使用来自癌症基因组图谱(TCGA)的数据库确认了有关KIF3C表达和生存分析的数据。通过对Oncomine的公共数据库的分析,研究了通过KIF3C调节肿瘤生长的潜在机制。结果低度神经胶质瘤(LGG)组(n = 20)的KIF3C蛋白表达高于高度神经胶质瘤(HGG)组(n = 33)的表达(P <0.05)。KIF3C高表达的神经胶质瘤患者的生存时间更长(P <0.05)。亚组分析表明,较高的KIF3C表达预示LGG组的生存时间更长(P <0.05)。这些临床结果与TCGA数据库中的结果一致。生物信息学分析表明,响应PI3K / AKT / mTOR途径抑制,KIF3C mRNA表达显着上调。
更新日期:2020-02-04
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