Centrosomal Protein of 55 Regulates Glucose Metabolism, Proliferation and Apoptosis of Glioma Cells via the Akt/mTOR Signaling Pathway.
Centrosomal Protein of 55 Regulates Glucose Metabolism, Proliferation and Apoptosis of Glioma Cells via the Akt/mTOR Signaling Pathway.
复制标题
中心体蛋白 55 通过 Akt/mTOR 信号通路调节胶质瘤细胞的葡萄糖代谢、增殖和凋亡
DOI：
10.7150/jca.15497
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发表时间：
2016
影响因子：
3.9
通讯作者：
Guo M
中科院分区：
文献类型：
--
作者：
Wang G;Liu M;Wang H;Yu S;Jiang Z;Sun J;Han K;Shen J;Zhu M;Lin Z;Jiang C;Guo M
前言：胶质瘤是人类最常见、最具侵袭性的脑肿瘤之一。胶质瘤的发生和发展的分子和细胞机制是难以捉摸和有争议的。中心体蛋白55(CEP55)最初被描述为一种高度卷曲的蛋白，在细胞分裂中发挥关键作用，但最近被发现在许多人类癌症中过表达。CEP55的功能在胶质瘤中还没有被研究过。本研究旨在探讨CEP55在脑胶质瘤发生发展中的作用及其机制。方法：采用定量逆转录聚合酶链式反应(QRT-PCR)和免疫组织化学方法检测CEP55的表达。采用葡萄糖摄取、Western印迹、MTS、CCK-8、Caspase-3活性及TUNEL染色等方法，探讨CEP55在胶质瘤细胞过程中的作用及机制。结果：我们发现CEP55在脑胶质瘤中表达上调。此外，CEP55似乎还调节胶质瘤细胞的葡萄糖代谢。此外，CEP55基因敲除抑制了胶质瘤细胞的增殖，诱导了细胞的凋亡。最后，我们提供了初步证据，CEP55的敲除通过抑制Akt/mTOR信号的活性来抑制胶质瘤的发展。结论：CEP55通过Akt/mTOR信号通路调节胶质瘤细胞的糖代谢、增殖和凋亡，其对胶质瘤发生的促进作用可能成为未来脑胶质瘤治疗的潜在靶点。
Introduction: Glioma is one of the most common and most aggressive brain tumors in humans. The molecular and cellular mechanisms responsible for the onset and the progression of glioma are elusive and controversial. Centrosomal protein of 55 (CEP55) was initially described as a highly coiled-coil protein that plays critical roles in cell division, but was recently identified as being overexpressed in many human cancers. The function of CEP55 has not previously been characterized in glioma. We aim to discover the effect and mechanism of CEP55 in glioma development. Method: qRT-PCR and immunohistochemistry were used to analyze CEP55 expression. Glucose uptake, western blot, MTS, CCK-8, Caspase-3 activity and TUNEL staining assays were performed to investigate the role and mechanism of CEP55 on glioma cell process. Results: We found that the levels of CEP55 expression were upregulated in glioma. In addition, CEP55 appeared to regulate glucose metabolism of glioma cells. Furthermore, knockdown of CEP55 inhibited cell proliferation and induced cell apoptosis in glioma. Finally, we provided preliminary evidence that knockdown of CEP55 inhibited glioma development via suppressing the activity of Akt/mTOR signaling. Conclusions: Our results demonstrated that CEP55 regulates glucose metabolism, proliferation and apoptosis of glioma cells via the Akt/mTOR signaling pathway, and its promotive effect on glioma tumorigenesis can be a potential target for glioma therapy in the future.